Grateful to you, to each of you that are here this evening, and especially to the wonderful speakers that will hear from tonight and tomorrow night. Thank you all for being here and thank you all for supporting this very important program. Now tonight we're going to hear about COVID-19, B's controversy, plasticity, epigenetics, and evolution. Tomorrow, Wednesday, February 16th at seven PM, we'll learn about concrete computer simulated evolution, ethics, and obfuscating science, among many other things. All in the context of Darwin and the legacy he left behind for scientists and for HUMINT. I'm very glad to welcome faculty from our college, the College of Arts and Sciences. And also from the University of Delaware has College of Agriculture and Natural Resources and College of Engineering. We also welcome colleagues from Delaware State University, from the University of Minnesota, the University of North Carolina at the University of Akron, and Duke University. These accomplished scholars will share their research and their expertise with us. So please join me in extending a warm blue ahead. Welcome to them. I know it's awkward to do that over Zoom. I never know how to quite get people to applaud, but maybe make, make whatever sign you think is appropriate there. About UT's Darwin days would not have happened without the enthusiasm and hard work and longstanding hard work of two people. Karen Rosenberg, Professor of Anthropology here in the College of Arts and Sciences at Udi. And John, john, Professor of Biological Sciences in Mathematical Sciences in the College of Arts and Sciences here at UT. Karen and John, thank you for all your work and planning this event for many years now. Thank you for gather especially an exceptional group of scholars for tonight, tomorrow's program. I very much look forward to two evenings of enlightening and inspiring presentations. It's now going to turn it over. And Karen and John mill tell us all about tonight's lecture is how you can participate in these events. Please join me in welcoming karen to John. Thank you. Thank you very much, Dean, blast scope at a real delight to have the support from the College of Arts and Sciences and the sigmas i international scientific honor society. And tomorrow night will be very much joined by Morris library. So please join us then as well. It's, it's my delight to introduce Professor Derek Scott from Dell state. That famous Shea usual situation is that you have to go way to learn about what's happening next door in this time of COVID and reading so many articles. An article appeared in Journal of the American Medical Association, one on COVID. And there was that Adele state and an amazing experiment had happened that in light of COVID, that they opened up despite the vaccine's not coming up. But with social distancing, masking and contact tracing, they were able to show that their students were far better, safer being on campus than being in the general population. It's the work of Professor Scott and his colleagues. He's a director of their molecular diagnostics lab, and he has a background in molecular evolution. And I was delighted to read his dissertation, even had phylogenetic trees that he had built. So without further ado, it is my delight to meet and introduce Professor Derek Scott from Dell state. Thank you very much for practice. Can you guys hear me? Thank you for the invitation. Duffy, delighted to be here and I'm going to try my best to keep too much time. Very much excited to talk to you guys. And you mentioned my previous work and it really occurred to me to allow the work that I've done in my previous stops in academia has been influenced by evolution. So I want to touch on briefly a little bit of that while I get to the COVID-19, which is the main part of the talk. And and I notice it's not face-to-face. So I always like to start at least my presentations, especially in a virtual setting, just introduced myself and I kinda given a foundation of who I am and how I came to be where I am. And so let's go ahead and get started. And I'll get to the name of the talk later on when we get to that section. But I said I'm Derek Scott, born and raised from Farmville, South Carolina. Isn't a low country near the coast and south Carolina and I went to high school and Wade Hampton and I was very interested in science, but I really didn't know exactly what I wanted to do and kind of what that look like long-term. But I didn't get a scholarship to attend Virginia State University. It's an HBCU in Petersburg, Virginia. From there, this is my freshman year as a biological science major. And this is the first time I really started to lay the foundation of really what I wanted to do in terms of science. Introduced to a lot of great professors, their average annual State University. Then I kind of still didn't know exactly what I wanted to do, but I knew I had to be in science and so fast-forward a few years and I graduated from Virginia State University and even OSI model in this picture, I had no idea what I was going to do as soon as this graduation ceremony was open. I had an internship lined up at Virginia Tech, but I really didn't know what my future held. I just kinda knew I wanted to do science. And from that time in that internship, averaging attack joined their program and the Department of Biological Science sciences for my master's degree. And I'll also talk about a few seconds to talk about the work I did there from our but thesis and saw studied abs. So T2 was a genius in all scenario. Breast is the coda is a fungus that attacks a lot of cabbage colleague greens, kale, broccoli, Brussels sprouts. Those types of plants are really affected by alternate your breast colon. And this is when we first use some next-generation sequencing. It was 454 back in those days, not around anymore. But taking out this gene and we knock it out really has some problems in terms of how the virus I'm at, how the fungus could in fact different types of plants. And so here in this picture you have three circles. The bottom two are the wild-type and then the bottom right one, if the compliment, essentially you want to knock that gene out, our recombinant of the gene back into the mom mutant to in hopes of restoring that wild-type phenotype kind of as a control. And so as you see, once we asked you all to challenge the R mu ands in our compliment, the wild-type that the mutant that are knocked out that gene had some problems. And so we knew this was an evolutionarily conserved gene that was important for strength in the cell walls of the fungus. And so we've looked at it and plants and we put the wild-type and a ONOFF slot ALB here. We have a BSL T2, the compliment, and as you see, it looks just like the wild-type. And the middle. We have the wild-type on the left, but the mutant on the right, you can see that the, the, the fungus did not spread out. And then on the third picture, I figured that there was something that was not allowing the fungus to get inside the leaves. That's the last scratch, the surface a little bit, what a pin. And then I read, annihilated the mutants and the wild-type. And lo and behold, everything but actually increased virulence. No matter if it was wild-type compliment are the mutant strain. And so bigger there may be something going on with some structures that we couldn't see. And I looked at it under a microscope. And as you can see, an a, this is what a healthy app resource looks like. It kind of works like a whole butter attaches to delete them, pops a hole inside of it. And the virus just kinda injects a lot of enzymes to, to kill the plant. And then E is what the woman has looked like from my mutants. And they look malformed. And we realized that because as app or cerium was malformed AB SGLT2 is very important for how this app or sold me a hyper sorry, a form. And it started to look for little holes like the stoma inside the leaves to get us out the plan and ask why when I scratched it, it was able to really get inside the plant very efficiently. And because of this delayed response and getting into the plant, the plant was able to essentially make a challenged defense and able to keep the virus, won't get them thought that covalent to break the fungus from really going through as regular infection cycle. So from there, I left Virginia Tech and I went to the University of South Carolina, did my PhD there. And in this case I really got more deep and evolutionary analysis. And also in the next generational, next generation sequence in as well. And so first is, here is software call mob is able to look at the genomes of different types of organisms until you how similar they are. And in this case, this is E coli and salmonella. They're kind of related to each other, but you see they're very conserved in terms the colors and the length are, these rectangles look about the same? And that's what you would expect for bacteria that are still closely related. But this is kind of actors. These are actually two Kyla back to species strains and you see that everything is really, really scrambled up. And this is something that we really didn't expect to see. And we wanted to figure out, well why is this genome scrambling happen? The only downside is you only had three Kyla back there's that were sequenced. And so I had to seek was about five or six plus trained to be able to do with evolutionary analysis. So I won't bore you with all that on the next generation sequencing programs that we found. But we did have a couple of good papers I came from. This will be compared the different types of assembly about this and stick with the technology or a GC perished bacterial genome. And then that led us to look at the essential genome that was conserve among Kyla back there and a close cousin, Ruben de Bono species. And so what I'll get into deep, I just want to, Dr. John mentioned the trees. I think it actually had the trees make an appearance where we looked at any one segment CB for K31. And we used a couple of abundant monads as our groups. And we're able to tell what part of phage regions, cell wall cluster region 16 S of course. And also the ribosomal protein operands. They were conserved from the protein level and also at the DNA level. And kind of where this look back as it was evolving from the original strain which was anyone Taoism, which is our wild-type strain. And so I don't want to just kinda inform where a lot of this has kind of influenced in you and what I'm doing right now, which is why I'm going to get N2 and still wanna just South Carolina. I'm a doctor TO Scott. And from there we got married, had a family, and this is the picture in the middle. I gotta obey my picture. So this is about my daughter and my two sons, Chairman Jackson and Zoe. And then on the left we have young login to marry. My daughter was born last weekend, so I had three I have to get a new a new picture to kind of break the family photo. But now I'm at Delaware State University and my research at Delaware State before COVID. We're actually still during COVID as well, but especially before cold, it was in the biopharmaceutical fields. And so we are working on a project and we're essentially looking at genome and a phenyl predictions and Chinese hamster ovary sales. Hello, Chinese hamster ovary cells are the workhorse of the biopharmaceutical industry. About what 80% of all biologics, biopharmaceutical products are made at Joe's sales. And we're doing this project with Dr. Lee UDL. We also work with Clemson University and also Tulane University to pick this four-pronged approach to figuring out how to make the, these drugs a little more affordable. And a reason why they're not affordable is because Chinese hamster ovary cells when they start to grow and he's bioreactors. The FDA has these very stringent rules for what you can actually use to market to the public. If the genome starts to change it just a little bit, we have to doorway the entire batch of medicine. So of course, we have a highways trying over, which essentially means you have less product and the prices go up. So you have biologics such as a1x, Remicade and Keytruda. Very expensive, 2 thousand to $20 thousand per gram to develop. Humira growth about 20 billion in 2018 alone. And without assurance it's a $103 thousand per year. So what we wanna do is figure out why these genomes are so unstable at once. We can figure that out. We can allow more product than the vein and the growth process. And at the product goes up, the price should go down, and so on. I won't really get into a lot of work that we've done there. Because right when we were in the middle, it will be add the lockdown. And so of course, in a global pandemic in March of 2020, every day and kind of shut down. And we realized for the rest of the semester we're going to go virtual. But leading into the fall semester, we needed a kind of a blueprint data bring students back safely. And of course there was no blueprint, yeah, because everything was brand new. And so we ended up bringing students back with a few approaches with a lot of mitigation strategy. The social distancing and washing hands keep in a classroom not so crowded. And they also frequent PCR test them, which was the key. And we were working with testing for America at first, but then we realized that testing was expensive if we were sent and test out to California to get tested. And the turnaround time was like three to four days that you guys can imagine an account is campus is light-years in the past. So we ended up having a mutual problem with New Castle County where they also have problems with your testing program, where we apply for a grant and we were able to give $5.5 million to build are all clinical diagnostic facility and Delaware States Kirkwood campus up in Wilmington. And from there leading to the spring semester, 2021 until even now, started late 2020. We do testing for Delaware State, Lincoln, different governments inside Delaware and also Pennsylvania. But the key of all this was we were able to essentially keep students a form of their status in real-time because we had a very aggressive testing strategy. And I pride myself on same-day results at decoding that. So as soon as a student it was positive, was able to pull them out immediately, as opposed to three or four days later when the results would normally come. And so once we we did this for about a year and we realized that we had a lot of good data from this, this strategy. And we decided to write a manuscript about it. And so over the next few minutes, I'll talk about assessment. Assessment of a multifaceted approach, including frequent PCR testing to mitigation of COVID-19 transmission at a residential historically Black universities. So here's everybody involved with this from Australia thanks to Dr. Hox gene testing for America and everybody here at Delaware State, from our provost to our General Counsel, to our president. And so the importance of this project, I kinda touched on it earlier, was that COVID-19 posed an unprecedented threat. Be really we're in this place of not knowing. All the facts that we even though today. And then at the same time there was no vaccine to be shared. And so we ran to figure out what's the best way to do it. How can we do this in a state, Anna? And so this was kind of the importance of this study. And we realized we were in it for about a year. Yeah, a lot of great data to share. Nest or objective want to investigate the mitigation strategy with social behavior, which is, we started with letting the students know, hey, you know, at the end of the day, we're only as safe as you guys make us safe. And at that point we were emphasized and wearing a mask, social distancing, getting enlarge groups and things of that nature. And the students were very well, was it received very well in terms of our mitigation strategies, you also did educational interventions. Yeah, a lot of myths out there about how the virus was spreading. And so we educate our population as well. And I think the most boring thing was just frequent PCR test it. Because, you know, the, the biggest thing that we noticed is if you don't give somebody soon enough, every person can have up to ten people on depending on when they get their positive results. And of course it will spread like wildfire after that point. So we did this from August 2020, April 30th, 2021, Delaware State. And then all of the participants were faculty, staff and students that were on camp was about 2300 people that were then chose to come back to campus. Myths. The on the midst of pandemic and B day have a good bit of people stay home as well. But actually more the habit of people has brought about a 30 percent, 40 percent of the population, they came back. So we realized that we could kinda have a case study. Well, we can see it is we'll be doing effective compared to the state of Delaware and the surrounding communities. And so that was kind of our experimental design where we have all these students had this test them, yeah, this data. And we can directly compare that with the information has come out of the public health lab with the state of Delaware. So I mentioned is before we had our education and outreach about social distancing, masking and also handwashing. And then a COVID-19 test, the plaque assistant of twice weekly polymerase chain reaction. Even right now, there's not a product of study, but even this semester to come back in January, if you're vaccinated, Think about 90 percent of us are, but they aren't had to get tested three times a week. And those who are have to get tested isolating steel. And so of course, the Olmec product kind of made that a need for now. So those were our experimental designs and I want to talk about a lot information on his lap. I don't want you guys to read a lie. I'll just kinda go over with you in a, in a snapshot. But over here on the left is simply everything that we had in terms of weekly test and for delaware state, right. And we would do an upwards of 3 thousand tests a week. Back then. Nowadays we're up to about 5 thousand. And we're looking at the results for negative, positive, looking at positivity rates. And they compare and answer to stay wide positivity rate per 100000 people. And as you can see that we maintain pretty, pretty gray positivity rates even across the board. Now what density is right at the end of each semester, I think we kinda have fatigue with students just really being, really be in on, on eggshells in terms of doing the right thing. And we didn't see like small increases. They had begun until almost 4%. And the spring semester, even though for most SMS worried about 0.4%. So write it down last week or two, we saw a lot. And also at the end of the fall semester. And so when you look at the data here on our second chart, we have about it. This is interesting in and of itself with students, faculty, and staff, we had only about a 168 foot fall in a 267 in the spring. And we saw that for students to symptomatic with about 28% of all births at 72. And a faculty or staff was about 14 percent versus 86 for asymptomatic, but in a spray atomic kind of a kind of, I don't know why, but things are going to look a little different. All we had these different strains percolating. And this will go to that of our current and future aims that I'll talk about in a couple of slides. But the students had about 40 percent symptomatic and 60 percent asymptomatic upper back. When you snap with reverse, almost 60 percent were symptomatic compared to 40 percent. So we saw this view change in and symptoms for even the students and also faculty and staff, where the numbers rose sharply for both and also ended up being the majority for faculty and staff. And as bottom right chart is just a simple a simple graph that shows you in light blue are the state of Delaware and the positivity rate. Then you have the Delaware State positivity way at the bottom, where you can see that the strategies were very helpful in terms of keeping our prevalence low compared to the statewide numbers. Now one thing I will say is especially right here in December, as you guys know, being on college campuses, we don't have a lot of students in December. So those numbers are artificially low because to be honest, we just I think he maybe did a couple of thousand for the whole month in December where we can do to 1000 pleasant we do on a normal semester timeframe. So that's definitely something that a caveat because almost 0% positivity rate, and I just think it's because he doesn't have a lot of students on campus during that time. So conclusions compare with the state. To stay wide rates that are our campus positivity rates were about 4.4 percentage points lower in the fall semester, and then also 5.6 lower in the spring semester. And bottom line is, we saw that the students were about, our positivity rate was about six times less than what we saw in the state. And something that I'm very proud of, the work that we're doing to keep our students safe. And I think there are, you know, we were in a fortunate situation now we can able to get these fast turnaround time. Like for example, even for athletics when somebody got sick, you're able to pull football player out of the general population. We've saved the season in some instances because they were getting their results. It will give them in about 12 o'clock to us at the lab. And you have There's also about three o'clock. And before I even had their meat is our data students will already pulled out. And the students are already going to have to pull out of the general population. So that is what the conclusions are there. And then for future research, what I want to talk about is, right now we have about 600 samples. Now we've stockpile from false what late fall 2020 until now. And what we're looking at is we want to see you. I see these days when the data were asymptomatic. For us, we have the we have the vaccination that was prevalent and spring 2021. And there will be also have all this data that we can go through. And I want to see what strains, where effect in the population of the issue as he went duties this 12th, our team off period. And right now we're doing this project. Well, we have a mutation panel is where you may probes that are able to only identify the mutant strains of interested who started an Alpha and a B should be at about Olmec Brahma. Now, i'll, I'll check in with the lab to see exactly where they are. And from there, you want to kind of see if you can make these correlations between asymptomatic versus symptomatic will be Misty. And I had the DSU campus Compared to stay wild even nationwide. And then we also have Nation original sequence and we have a couple of next week's here that we can use to sequence these. And I'm going to have some strange that we just don't have any data for whatsoever. And then I'm just interested kind of see what they are. And so at that point, back to evolution. What have we got to evolutionary status in terms of how does viruses moving and changing and the populations on our campus specifically. And we also do have sample from the state of Pennsylvania as well. So this is some of my work is that the Codelab, the LDL. And I'll stay close to my 20 minutes. I didn't want to go over leave a little bit of top questions. But thank you guys for your attention. And I'll take any questions that you may have. Dr. Scott, thank you so much, incredible work and that kind of safety you've done for your students. And we've been joined by Dr. Neil Hox gene, year primary author of the article here in the audience tonight. Who alerted me to your wonderful work. And this is just truly, I think, a national story that deserves incredible kind of attention. And the importance of doing this kind of analysis. Do we have any questions from members of our audience? Please unmute yourself and ask a question. Dr. Scott, this is how are you doing? I'm doing. Great. Thank you for presenting that. I'm wondering if you just wanted to share how you were looking at CT values and finding very early cases, decoded, identifying them and having retested. Once I think things are down for their dogs time, read the paper. We're going to try to get out pretty soon where the advantage of work in I think Buber a small lab, a small lab we do about between 1520 thousand samples a month whenever we're movement, when the students populations are up. And so one of the important things of being a small lab is we're able to contact the health centers for the different universities, the HR departments or the organization that will be worked with and were able to look at I had to look at every single test that comes to the lab. And I had to look at it to see if the machines acting crazy, if it's actually a legit positive and then we retest them. So a strategy that I was able to figure out pretty early on is. Based on CT values, based on a EUA, we use a Yale saliva direct method. And based on their protocol, we can only call somebody positive if their CT value is less than 40, right? So at this point now in your positive, if it's 40, your negative. But of course I know you're not really negative. I know you're in fact, yeah, just can't call you positive. So what I would do is I will get in contact with the student health center to say, Hey, this person, he's not technically positive and I want you to bring that person back tomorrow. There'll be positive tomorrow. And then that will essentially if there was a Monday, that person theoretically wouldn't come out for testing until Wednesday or Thursday. But at that point, if we bring them back that Tuesday to get them out of the population quicker on two to three days average before they're able to do their next official test. And so we had a lot of success with that. We'll just stop. They will call back and it was a you write that person was positive and we're able to pull them out and get them from being involved in other parts of the student population. So I think that's a very powerful tool to use in terms of CT values where you could see the advection and you see that nice curve, but you just can't call it positive based on a protocol. Bring those people back in and and really get them to be to be tested way quicker than they would've normally otherwise it been tested. When last questions before we go on. Well, if not thank you, Dr. Scott, the incredible work on behalf of your students and your staff at not only del state and Lincoln, but setting a model for us nationally that is truly incredible work and showing the power of the, you know, kind of how evolution relates to contact tracing in terms of how this medians are evolving over time within a local population. So, thank you so much for sharing your work where you simply delete it. So Professor Rosenberg? Yes. So thank you very much. It's my pleasure to introduce our next speaker who was debride the lady, She's an associate professor in the Department of Entomology and Wildlife Ecology here at the University of Delaware. I've actually wants to meet her for a long time because we shared a student a few years ago, an ISA speak when he used to tell me quite a bit about about the work that she was doing. Professor Dwayne, He's worked on pollinator health and productivity. Just 30 years of experience studying pollinators, specifically honeybees. And she maintains a 100, one to 200 colonies in Delaware, Maryland, and Pennsylvania. Thank you very much for coming to Darwin Day. And here's Professor Delaney. Thank you. Can everyone hear me? Wonderful. I'm going to share my screen and we'll get started. So I was asked to speak on Darwin's theories. And there's so much to talk about because Darwin was fascinated in like a good way, in a bad way, I would say by bees. So it's, we're going to talk about the diversity of course, because we can't not. But I did want to start out with a quote from Darwin. And it is not the strongest of the species that survives, nor the most intelligent, but the one most responsive to change. And that's going to be the theme of this talk as we go through and kind of look at how he observed and scientifically reasoned just through observing the behavior. And really, this all started in the 130s with his observations and it's scientific reasoning and his notes and journaling on the HMS Beagle and kind of going to these areas in the world that had such incredible diversity. Such incredible diversity that he had to think about why there were so many different kinds of one particular type of animal. And so as we move on and kind of think about how he was developing his ideas and his concepts. And when he was writing the book, the Origin of the Species and his idea of evolution through natural selection. We have to think about these ideas of variation, inheritance, selection, and time, which are the main components of this natural selection, this evolution by natural selection. I'm sure you've seen many different cartoons of natural selection in action with the giraffe is probably one of the more famous ones. Um, and so this idea that over time, individuals will get different mutations and ones that are favorable and adaptable will actually be inherited by offspring. And that will kind of slowly, organism will change over time in response to the environment and changes in the environment. But there has to be genetic variation in order for this to happen. So social insects and bees are a big part of this perplexed Darwin. And they can confounded his mind so much that it actually delayed the publication of The Origin of Species for over two decades. And it was really just kind of this crunch time, even though he was still perplexed, but he, other people were also getting ready to publish on similar ideas. And so there's a lot of interesting things to think about as this man is coming up with this way to explain the diversity that we see on this planet and the behavior of bees, social insects. Basically, the order Hymenoptera in general basically was making him very confused. So let's kind of look at this a little bit. Darwin's Dilemma. And the dilemma is displayed here. What you're seeing or worker bees, and what they're doing is they're festooning. That's one of my favorite words. But they're festooning and they're measuring, and they're building cone. And it's this behavior, this kind of group behavior of these bees to make these very complex, amazingly efficient shapes. The hexagon, which if you know anything about hexagons, it's one of the strongest shapes. It's the most efficient shape and start in terms of storage and the fact that they build and these shapes. How did they learn this behavior? How did this behavior evolve considering workers are sterile, right? So this was the big conundrum here. And really he focused on homebuilding because he was able to look at other social bees and find certain b's that make circles, certainties that make different shapes. And so this was important for him and trying to work through this problem with sterile insects, social insects being able somehow to evolve complex behaviors. It's very interesting. So how do sterile cast traits evolve or get passed to the next generation? Well, one thing to think about is a queen honey bee lives in a very stable environment. She's groomed, she's taking care of, she's fed. Yeah. She has a hard job of laying lots and lots of eggs, thousands a day. She has a pretty temperature regulated environment. There's not a lot of selection pressure on her. However, workers are going out and foraging. They are dealing with maintaining a temperature in that HIV. So HIV does die or desiccate. They are under complete selection pressure because they are dealing with a changing environment. So selection pressure is going to be strong for these sterile workers. But how does this work? How did these traits get passed on to the next generation? Well, later, more information really started to explain this. And it's this idea that basically most and actually all Hyman doctrines are haploid, diploid. That's how their sex is determined. And what I mean by that is if we look at a queen and she were to be mated, and she decides to fertilize an egg, she can decide that she will then create diploid offspring. If it's deployed, then it's going to be female and it will either be turned into a worker or it can turn into a queen. If she does not fertilize that egg, then that offspring will be haploid and that will result in a male offspring we call a drone. Now this is really important because this basically determines whether it's going to be a worker or a queen or a drone. Now, what determines whether it's a worker or a queen? We'll get to in a minute. But let's unpack this a little bit more. The other piece of this puzzle is that if we look at a queen honey bee, when she mates with the drone, she mates with many and she stores their sperm in a special organ in our body. And so then she can actually lay eggs and she fertilizes them and she creates these workers here. Now, the thing I want you to take away from this is that basically the daughter and the mother share about 50 percent of their genetics. However, the worker and the worker, so sisters share 75% of their genetics. So why do we care for many of you know, in Hymenoptera, daughters are more related to each other than they are to their own mother or father. And so this makes it worth giving up reproduction because actually they're helping the queen lay more of them. And actually they're helping the queen possibly and eventually lay other queens that are more related to them. So let's look at this a little bit more. Caste differentiation. In honey bees. Particular it, It's different if it's an aunt or if it's a stemless be even they actually in honey bees, worker development or, or a queen development is decided through differential feeding. These are worker, I mean, excuse me, these are queen larvae right here and they're bathing in pools of royal jelly. And it's called royal jelly because it is very protein-rich. Deploy larvae before they have been decided to be worker or queen. Once they are decided based on cues in the colony and in the environment of the colony. Those larvae will be fed more food as well as a higher-quality food. That's higher quality food. And this increased amount of food will change the genetic flip and physiological switch to a queen trajectory of development. So that's pretty interesting, right? So if we unpack all of this, we see that newly raised virgin queens will be 75 percent related to the workers in that colony. And when they leave that colony through swarming, which we'll talk about in a minute. They will carry those genes forward and propagate them throughout the landscape. So as we think about swarming, this is reproduction at the colony level, which I think is one of the coolest things about eusocial insects. Not only do they reproduce at the individual level or the queen does, but the colony reproduces the whole, entire colony. So essentially, we have a colony of bees. And that colony of these will get very crowded. And that crowding signifies that they need more room. They can't smell mom anymore. So they start making new virgin queens. Once those virgin queens actually start to ripen and hatch out, that's when this colony level reproductive event occurs is called swarming. And about 75 percent of the colony, the workers and also the virgin queen stays in the colony, but the old queen leaves the colony with 75% of the workers. So I have a little diagram here to show you. Let's see if I can get it to work. So here's the parent colony, Right? Connie gets too big. Virgin queens are raised once they hatch out, the old queen and three fourths of the colony will swarm. And a daughter colony will be made. The queen will get mated. She'll, we'll head up this next colony by laying eggs. So that's how the workers genes get propagated to the next generation. Very interesting and complex. Now, I also wanted to touch on Darwin's botany and his love of the humble B, which we call the bumblebee. Because that's another part of Darwin, his love and obsession with bees. And between 840 and 880, he actually published close to a dozen books and a lot of journal articles about different botanical topics from insectivorous plants. But she was really kind of obsessed with plant reproduction, which is pretty darn knee. And the first plant that he really started to do work, these are actually drawings from his sketchbook. Was prim ELA, the primrose. And what he found is that Primrose actually has two different types of styles. This is called diastole, right? And so there's this long variation here of the style, and then there's a short variation. So you can see the answers on either side. You can see the answers up here on either side of the short style. So this has major implications for getting pollen to be moved to the right reproductive part. So pollination can occur, fertilization can occur. And so this was the beginning of his kind of obsession with variation in plant morphology. And then also how that relates to variation and plant visitor or flower visitor morphology. So if we look a little bit, we really see through his work on his botanical kind of facet of his life. He was really interested in co-evolution. And this is a quote from him. Thus, I can understand how a flower and a B might slowly become either simultaneously or one after the other, modified and adapted in the most perfect manner to each other by continued perturbation. Preservation, excuse me, of individuals presenting mutual and slightly favorable deviations of structure. That is just beautiful. And what you see here, this is a bumblebee. And if you've ever see a bumblebee on Beard tongue or pens to Min, and that's the scientific name for Beard tongue. It, you see that they co-evolved. They fit perfectly. It's almost like pens to men. Flower Corolla is as little sleeping bag for that bumblebee, perfectly made for it. And so if we think about why there is this close connection, specifically between bees and flowers, there's lots of amazing mutualism. But I'm going to focus on bees. And it's because bees absolutely require floral rewards for all growth and development. Nectars, they're made carbohydrate source. Pollen is their main protein source. And so they are completely dependent upon flowers as their grocery store. And so they need these types of nutrients. Specialize to visit flowers and they're specialized to figure out how to get these floral rewards. And some flowers can be pretty darn tricky. Here we have an end, granted, this is a little mining be and is covered in pollen and it's going to go back to its nest in the ground. And it's actually going to room off on its pollen, make a pollen ball and lay an egg on it. And so this is actually a very early instar, almost still an egg larval stage of this M trend and the daughter. I can't tell if it's actually a male or female of this, this mining be. So many flowering plants depend on bees for pollination. And not just B's other flower visitors to. But like I said, we're going to focus on these. This is a mega CG-islands and you can see this is the abdomen here as covered in pollen. You can see how wonderfully at once it visits another flower. If it's going to visit the same conspecific flower, is going to transfer that pollen, which will then be pollination, which will then hopefully cause fertilization further on down the road. Here are some other pictures of bees specifically intimately interacting with flowers from this bumblebee covered in pollen here, to this honeybee visiting facil yet snack the folium, which is a beautiful plant that has purple sparkly pollen. You can see it packed on its cubicula here. And this bumblebee here kind of working the curl of this particular flower and touching the anthers. So this quote really kind of explains that flowering plants pollinated by insects reveal more of their genetic diversity in their blossoms than in any other of their organs. And this is really important because that's what I was talking about. If there's variation to be played upon this that they'd been playing upon each other. Flowers and the flower visitors they've been working in. And we're going to look at some examples of this. Flowers have been shaped by visitors and the Hoover time. And if we look at just the family run Anki Lacey, here, you can see the diversity of colors, the diversity of flower shapes, how the flower actually is attached to the rest of the plant itself. All of these are going to affect the interaction that a visitor has with that flower, how it needs to actually interact with that flower. And here are some more, just the diversity and shapes of different flowers. Now if we break them down, radial flowers are very common. These are broad landing platforms for different types of flower visitors. So they attract all different sorts of flower visitors and they have easy access to the nectar generally and also to the pollen. If we look at other flowers like this one, this has bilateral symmetry. And because of this bilateral symmetry, and it kind of is in a long plane, there's not really a landing platform. So visitors have to learn how to handle that flower, how to kind of fly around it, how to hold on so that they can access the nectar and pollen. Here's ones with pendant habit. And so this is very challenging for a lot of different flower visitors, butterflies and other types of visitors are going to have a hard time holding on and getting their mouthparts into this flower. We have bold flowers like hello boars. And you can see here these are actually the sepals, but the true petals are these green little cones that have been modified and trajectories. So that's where the nectar is. And what's really interesting is we have the anthers with all the pollen right above it. So you can imagine that the visitor coming in, going into that nectary and then being doused with pollen. And then tubular flowers. Tubular flowers are often associated with insect pollinators because the length of the tube of the flower is associated with the length of the tongue of the visitor, which is awesome honestly. So now if we kind of combine tubular with bilateral symmetry, we have one of the most complex types of flower designs. And the position of the nectar is more complex here. So really, these require specialized types of visitors, ones that know how to handle the flower in order to quickly access the rewards. Salvia being a great example. Now, this is kind of interesting to this plant here. There's actually two different ones. But both of these, this is a Brazil nut and this is a larger stroke. Yeah, legis drum yet. And both of these produce what we call fodder pollen. And what they do is these anthers down here, you can see these are longer and they've already D hist or really. Pollen. Those produce pollen first, but it's not, it does not have reproductive value. It only has nutritional value, but it causes recruitment to the flower. So once recruitment to the flower by visitors happens, then they start to release their reproductive fallen. So this is a very clever evolved behavior of this flower morphologically end behaviorally to actually increase the occurrence of, of pollen movement of a visitor coming in contact with fertile pollen and moving it during the correct time, which I think is so amazing. All right, and then of course, flower features like nectar spurs, definitely shaped by visitation. Some of these are so long, these are column binds here, but we also see nectar spurs in orchids. And we can most imagine that these nectar spurs, they hold nectar and of course, the proper visitor is going to have a tongue that matches the length of those nectar spurs. And that has been shown again and again, probably one of the most exciting examples, I think I have a picture in the next few slides. But also the position of the reproductive parts here, anthers, I think this is a lily. These anthers have split open and are releasing or the hissing pollen. But different flowers have evolved different locations of where the division or these, these anthers open and split and release the pollen. So you can imagine the visitors coming in. They're going to handle or interact with that flower in a particular way. Depending on kind of where this decision or direction of the anther slit is going to be positioned. Now, a really interesting thing when he was doing his work with, with humble bees. Not only did he see this kind of coevolution between the humble B and the flowers at visited. But he also found some cheating. And he coined the term nectar robbing, which I think I didn't actually even know that. Uh-huh. Because he witnessed humble bees actually going to the base of the Corolla and drilling holes. And their goal forgoing the natural design of the flower. And this is a quote from him that circumventing the flowers natural design. So this visitor isn't doing anything for this flower. It's actually robbing its nectar and not coming into contact with the reproductive parts at all. And this was all through careful observation. So now let's take a quick peek. Me just check my time and how visitors shaped morphologically have, how they've been shaped morphologically and behaviourally buy flowers. And so we can just see here in size from mega Kylie Pluto Wallace's be with this 2.5 inch wingspan to predetermined medulla, which is two millimeters. So very, very, very different sizes associated with flowers. Also uh-hmm. Of these different sizes. Also body hears of bees. They're branched specifically so they can pick up pollen, which is pretty awesome. Also tongue length, this is probably one of the most obvious examples where we see the different lengths of these tongues and how they're associated with the different flowers. They actually get their nectar from. An orchid. Bees having these extremely long tongues. Here is an example of a very long proboscis of a sphinx moth. And you can, they found this Madagascar star orchid and they knew that the moth had to have an extremely long PRG, a Bosque isn't it took a long time to find it. But they did. This is crazy. And this is a picture of a ground b and drain a lot, Sarah. And this is on a particular flower, and you can see the B, it actually opens up the bind the flower bud, and then it goes in and extracts the pollen. But what I want you to see here is this crazy mouth part. It's just starting to open here. You can see a nectar droplet there. And then it even unfurls even more. So it specifically can get all the way down into the Corolla to get the nectar. So it has a mouth parts specifically designed to be able to get the nectar and come into contact with the pollen. It's amazing also that the trichromatic vision and the fact that bees can see UV. This is something that flowers. When you look at them under UV, they look like a completely different flower and they're telling bees where the rewards are located, which is amazing. This is the same flower with regular light and with UV, same here. You can see the nectar guide showing where the floor rewards are. This is a minority under UV, kind of showing the beauty and what a bee might see and where it can go to get its floor reward. And the antennae. I could go on and on, but I think I'm pretty much out of time. But there is, so, there are so many different morphological adaptations that visitors have to be able to effectively visit flowers and collect pollen. And the squash be itself being able to utilize and actually not only use the pollen, but rendezvous and made inside the flower itself. All right. I probably don't have any time for questions because I think I went over and I apologize, but I hope you enjoyed and what a wonderful way to commemorate Darwin's work, listening to all these people. So thank you so much. I have a question. If anybody has one or two questions, I think we can pick them. Anybody. If you have a question, just speak up. Okay. Well, I think I'm John, to introduce the next speaker, trying to unmute myself here. So thank you. Thanks so much Debra. Such beautiful work, but it's my distinct pleasure to introduce Professor Mark Borello from the Department of Evolution, Ecology, Behavior at the University of Minnesota. He's the director of their program in the history of science, technology, and medicine. I was particularly drawn to is University of Chicago book on evolutionary restraints, the tenuous history of group selection. And I actually asked Mark to address a particular statement that he made in his book about the importance of the kind of controversy that has been lasting over many years on group selection for our students. So without further ado, it's my delightful pleasure to introduce Professor Mark Barilla from the University of Minnesota. Thank you, Mark. Thank you, John. As everything projecting correctly, Are we good? Okay. Well, I I want to thank both John and Karen for organizing and all the folks behind the scenes and and also Derrick and Deborah for really nice talks. Prior priors, mine. As John suggested, he said like, Hey, on page 170, 155, you said x, like, can you defend that or can you talk about that? So I thought, Great, I'll try to do that. And so basically what I want to do tonight is just talk about a couple of episodes in the history of science. Some people think, Oh, we should stop talking about Darwin. What about Mendel? Some people are obsessed with Mendel. You know, some people have other kinds of scientists that they love or ideas that they love. But, but I think that like, you know, Mendel deserves some attention. But, but, but tonight is for Darwin. So here we go. I'm going to talk a little bit about, again, these two episodes. One is this episode of debate over what I'm going to say. It's the tempo of evolutionary theory. So the debate over punctuated equilibria. And then the second one is a debate over sort of the level at which natural selection acts, right? So does natural selection act on genes or does it acts on traits, or does it act of organisms to act on? Populations are superorganisms. And so, and I'm going to take a historical approach here. I am not a biologist. I, though, I studied biology with John as an undergraduate. I'm a historian. So here we go. Let's see. So, so Steve Gould is the Stephen Jay Gould paleo biologist at, at the universe or at Harvard University, is the source and inspiration for the talk. It's 2022. And Gould died in 2002, so that was 20 years ago and published structure of evolutionary theory the same year. He also published a very influential paper that I'm going to talk about tonight in 972 with his colleague Niles Eldridge on punctuated equilibrium. And so we'll talk about that in a minute. But, but what they wanted to do in that 972 paper 50 years ago was, was to contribute to this ongoing discussion regarding the rate or tempo of evolution. Like how fast is evolution happen and does happen at more of, more or less of a constant rate. So Darwin, influenced by Charles Lyell and his ideas of uniformitarian geology, was very sort of committed in many ways to this, to this kind of gradualist approach, right? What I'll refer to later as phonetic gradualism. But even early on, some folks were concerned about this, including Huxley. So in some sense, schooled and Eldridge are echoing a concern that was raised by Darwin's advocate and ally Thomas Henry Huxley, a comparative anatomist. And Huxley in a quickly kinda scribbled note that he sent to Darwin the day before Darwin published The Origin. He wrote, you have loaded yourself with an unnecessary difficulty in adopting NetTutor non-fossil Sultan, so unreservedly. And so for those of us who, who may be rusty with the Latin, not to a non facit Southam means nature does not make leaps. And Huxley were saying like, maybe in nature does make lead sometimes. And he was warning Darwin off what he saw as kind of an over commitment to this idea of gradualism. So let's jump to 972. And in some sense, Gould and Eldridge are echoing this concern raised by Huxley right there. Oh, I've patois. They're arguing for this reconceptualization of the paleontological record. They argued that the view of file let it gradualism, this kind of idea that things change constantly slowly. It's all small gradual plane change leads to the wrong expectations and the wrong focus. And so that's the claim on the preceding slide that, that early slide that stasis is data. Like we shouldn't just look at the periods of change and evolutionary history. We should also look at the periods of stasis because that's an important part of the phylogenetic history. So they say We need to look at these extended periods of time where we see very little morphological change and to properly understand the phylogenetic history of whatever lineage we might be interested in. And what's interesting from a historian's point of view. And what the debate tells us is about the process of science, right? In 1972, they were Gould and Eldridge responding to what they saw as an increasingly unrealistic characterization of evolutionary theory, of Darwin's theory. And one that had really occupied, again, dark biologists going back to Darwin, including Huxley in the little quote that I, that I highlighted a minute or two about. But we can see if we look at so, so on the left here we have Gould and outages diagram from there, 1972 paper and on the right here, the only illustration from the origin and 859. And we could see from Darwin, Darwin's diagram that most of these lineages were almost constantly gradually changing. There are a couple of lineages that look like, well, they don't change so much, right? But most of them, most of the history, most of the evolutionary story is the story of gradual, constant kind of change. But, you know, when we look a little bit more closely at the text of the origin, we see various places where Darwin was a little bit more maybe open-minded. So, for example, on page 314, Darwin writes, despite the fact that the diagram looks pretty gradualist, he seems kind of open-minded here. He writes, I believe in no fixed law of development causing all the inhabitants of a country to change abruptly or simultaneously, or to an equal degree. So there's variation in the tempo here, right? Things, things change at different rates for different populations, for different contextual reasons. As the theory of evolution or the theory of descent with modification developed in the 20th century through the mathematical modeling the path population geneticists among others. The emphasis on gradualism was, was, was increasingly significant. And so by, let's say 1963, when Ernst Meyer is writing animal species and evolution, a major text in the posts in this era. He writes, the proponents of the synthetic theory maintain that all evolution is due to the accumulation of small genetic changes guided by natural selection and that Transpacific, so higher levels, species level kinds of evolution is nothing but an extrapolation. The magnification of the events that took place within populations and species. And so what's interesting here is you can see Eldridge and Gould are responding directly to this kind of a claim that Meyer is making in 1963. And I think again, there's a, quite a bit of controversy generated over this idea in the 1970s. And we see sort of this going back and forth, looking back to Darwin. Looking at sort of again, the development of the mathematical models developed by the population geneticists starting in the late 20s and 30s and 40s. And then coming to this kind of, you could think that, that Myers view is the kind of canonical view. And then we have these two young paleo biological upstarts challenging Meyer and saying No, no, no. It's, it's, it's, it's, it's different than that. There are these long periods of stasis that we need to pay attention to, that, that there's not sort of a constant or equal rate of evolution. And, you know, Gould and Eldridge use some of the quotes from Darwin himself to say, look, we've departed from what was a more pluralistic kind of a view into this much more kind of narrow point of view. And of course, interestingly, you know, these things shift back and forth among evolutionary biologists within sorted the teaching of biology at various levels where it's at, whether it's at the university or at the door at the high school level. But one of my favorite quotes is from Doug for cima, an evolutionary biologist at suny Stony Brook. And, and, and Fatema when he was reviewing some of Gould's work, and this was back in the 70s. He said, he wrote, history will teach us if nothing else, that most in, most ideas in science had been wrong or at least very incomplete. And that most scientists have worked within a framework of assumptions that have proved false or inadequate. Ensure history should teach us humility. And I think what footie men saying here is quite consistent with what Gould argued when he talked about sort of the uses of history and the value of controversy or heresy in, in, in scientific debate and in the scientific process. And for my, for me as a historian, my experience exposing your students to controversy and debate in the history of science allows them to consider that the information in their textbooks has not always existed. We know of science is the product of people like them, like the students themselves, working to answer questions similar to the questions that they themselves might have. And one of the most successful ways I've found to engage students in the history of science is kind of by looking at the historical roots of these debates, right? So that's punctuated equilibrium. If you're interested in this topic, There's a ton of work out there. My friend and colleague David Sapolsky has written a book called re-reading the fossil record that talks a lot about the development of these Paleo biological ideas in the 1970s and then into the 80s, 90s, and the 2000s. When John asked me to give the talk, I myself have worked on this. Another question which is a little bit more about mode, the mode of evolutionary change. And I focused on in my book, in some other papers on the history of what's called group selection. So one of the other questions for Darwin, and I think Debra's talk, you know, the social insects world of deep interest and concern to Darwin is connected to this. Was this question of cat. Does natural selection act on. So we didn't have, he didn't have, they didn't have in the 19th century genes. But do, does natural selection act on traits, parts of organisms? Or does it act on whole organisms? But does it act on groups of organisms? And those might be families or communities or clans. Darwin use lots of different language. Or can it act on species? Is it for the good of the species that evolution is working, right? And that has been a controversial notion again since Darwin. So much so that various folks have, have sort of presented in different ways. This is a graphic from Seed magazine, which is kind of a science interests magazine. And you can see on the I mean, there's a bunch of different ways you can do history of science. Here's a, here's a graphic version of the story that I'm going to tell Over the next section, we'll talk. And again, I'm going to try to keep that thing, but what, I'll give you a quick walk through the group of the, the curve of group selection, right? So you can see over here on the vertical axis the concept, the scientific concept can go anywhere from wrong to like one for the history books and in-between there's on the covers of magazines, trip to Sweden for a Nobel textbooks cited in her article discussed with colleagues and then scribble on a napkin. And starting with Darwin, and it starts out just below scribble on a napkin. And they credit Darwin with some sense that maybe, maybe group selection as part of this evolutionary process. And then there's Samuel Morton Wheeler, a Harvard entomologist, again, focusing largely on ants, but a social insect who talks about superorganisms and selection acting on superorganisms. This was in the 19 teens and up into the 20s. By the middle of the 20th century, group selection is on sort of a downward curve. That is sort of really starting to plumb it when William Hamilton comes up with the notion of kin selection, which focuses at selection at the level of the gene. But explains how, again, as Deborah was talking about the bees, haplodiploidy might be, might explain at the genetic level this kind of group beneficial traits as a byproduct. This is echoed by GC Williams, adaptation and natural selection and then so on and so forth. What's interesting is that it can of, here it reaches its new dear. I would have put them a little bit later with Richard Dawkins around 1976 and I'll talk about him in a second. So I would have made that went even lower. There you have it, right? So, so let's try to work through this. This, this sort of, you can see that this represents some kind of a controversy, right? Because if this is the scientific opinion of this idea, it's kinda all over the map. And I think the other thing is that it's fast. It's, it's interesting that they get the visual wrong at a couple of points, maybe starting with Darwin. But there's an interesting tie-in here. There have been lots of popular articles over the years that have argued that we should stop talking about Darwinian evolution. Science like forget about the past. We don't need Darwin anymore. But again, as a historian, I respectfully disagree. I think that having a nuanced understanding of how Darwin's original formulation of the idea of descent with modification was formed and then tracking those changes that the theory has undergone in the subsequent 150 years can inform contemporary debate. It can, it can, it can really help us think about the fundamental conceptual issues. And it can even, I would claim, provide guidance for future research. Okay, I think I'm on track here. By my calculation, I have about six more minutes and I have about four more slides I should buret. So, so there's that though most people agree that Darwin really did focus in the origin on individual selection acting on individual organisms. The passages that I have here indicate that there were some phenomena in nature that were more suited to an explanation that invoke selection of communities or groups. And so in the origin, he's talking about like, you know, we can perhaps understand how it is the use of the sting. And here we go back again to the bees. That should so often cause the insect's own death. For if on the whole, the power of stinging be useful to the community. It will fulfill all the requirements of natural selection, though it may cause the death of some few members, right? So again, he's thinking that selection is saying communities that have the altruistic or the self-sacrificial members will be better off as communities even if they lose those members. And again, here we're pre genetics, pretty haplodiploidy, all of that stuff. And then in The Descent of Man, in 1871, Darwin shifts to talking about humans. And he says, it must not be forgotten that although as his standards of morality gets but a slight advantage to each individual man and his children over the other men in the same tribe. Yet that an advancement in the standard morality and an increase in the number of well-endowed men will certainly get an immense advantage of one tribe over another. So here a cooperative group of humans, group that is practicing mutual aid, that is morally sort of looking out for each other as opposed to constantly battling and competing for resources, will be the more successful community, right? And perhaps more significantly this question of the level at which natural selection acts immediately for Darwin raised questions about the evolution of morality. Like even in a 2008 book, The Invention of altruism, historian Thomas Dixon. He claimed that the explanation of sociality, the source of moral behavior for Darwin, was one of Darwin's primary goals. He really wanted to understand how evolution might inform what we ought to do, what is morally right. And, and indeed so elevated was that moral tone of Descent of Man that Darwin wrote to his daughter Henrietta, who was editing, reading and editing the manuscript and 870. And he wrote her a note. And the quote is he said, who would ever have thought that I should turn parson? So here's, you know, the, the, the blast theming materialist talking about moral behavior. So again, this is just to point out that Darwin makes room for natural selection acting on communities or groups. And even some of the architects of the modern synthesis where population genetics is incorporated, mathematical modeling is incorporated into evolutionary theory and it's largely focused at selection acting on individuals and genes. Someone like Theodosius Dobzhansky, population geneticists in his, in his text, genetics in The Origin of Species, played some role in thinking about group selection. Various folks including a British ecologist, Bureau continent when Edwards pay close attention to the shots, He's idea balancing selection. This is the idea that natural selection has to balance between purifying a population to a particularly fit genotype and maintaining sufficient variability in the population to ensure the long-term survival of the population. And so in genetics in the orange species, dumb chance, he writes, evolutionary plasticity can only be purchased at the ruthlessly dear price of continuously sacrificing individuals to death from unfavorable mutations, right? So again, this idea that maybe selection is acting on this higher level, the group level. But the increasing consensus, postmodern synthesis of modern biologists was the mechanism of natural selection was focused on individual organisms. I'll just say a quick word about the ecologists that I just mentioned, Bureau continent when Edwards, who spent a lot of time thinking about group selection and arguing that group selection was important, particularly in his 1962 book. But this is a passage from a paper that he presented in 950 five, that outline the theory that he would spend the next 40 years until he died in his nineties. And in the nineties. Defending, he wrote a collective response by a social group 2. Two, general conditions of food productivity does not appear much more abstract and improbable than the corresponding individual response by male birds cleaning territory. The theory that a slowly breeding birds have evolved, a series of adaptations, giving them control of their numbers permits a rational explanation of hitherto unconsidered or anomalous features of breeding birds are breeding biology. So if on a Darwinian kind of calculation or on the individual level kind of calculation, all birds should be trying to make as many offspring as they can. How can we explain that the gantry here in, in Newfoundland, where the birds restrict themselves to this one stone outcropping with a little bit of the colony here. And when Edwards argues that this is a function of selection on groups maintaining populations below the level of resource exploitation. All right, I just have a couple more slides here, so I'll try to go fast because I think I'm getting close to my time here. Most of us here at a Darwin Day celebration have heard or read or know something about Richard Dawkins 1976. Like literal bestseller. It's hard to write an evolutionary bestseller, but Dawkins Did it. It was also intellectually incredibly influential in terms of how people think about evolution. Happy people think about evolutionary biology and how they teach it, and how they research it. And of course, no one was more opposed to group selection than, than, than Richard Dawkins. He argued, following the developments in evolutionary genetics developed by RA Fisher and WD Hamilton, that natural selection acts primarily on genes. And that cooperation and altruism could only evolve if they benefit the individual or the individual's relations. And so he writes, be warned that if you wish, as I do, to build a society in which individuals cooperate generously, you can expect a little help from biological nature. Let us try to teach generosity and altruism. Because we are born selfish. These kinds of passages run throughout the selfish gene and in the mid seventies created an intellectual environment where the invocation of group selection was deemed heretical. Dawkins, in his highly influential book, aimed to give full voice to the criticisms of species, good of the species. Arguments that were presented by people like David Lack and George C Williams. This sentiment was echoed by many others in the community of evolutionary biology. Though the debate was not completely abandoned. And Gould, in his final book, the one that I mentioned at the beginning, published in 2000 to the year that he died of brain cancer. In his last book, Steve Gould wrote that when Edwards claim for group selection may be wrong. But I can say few other theories presented within evolutionary biology during my career that could be deemed so challenging implications, so comprehensive in claims, and so fascinating in extension, and so thought-provoking. So Bob Dylan also wrote, wrote lyrics that was called, There's no say it. That way where he wrote, there's no success like failure. And I think there's something to that in failing, in the, failing with this theory when Edward succeeded in shaping evolutionary research for a couple of decades towards a more individual level, folks who responded negatively to the claim and they focus even more intensely at an individual level. The science of genetics was developing and, and pushing more focus in that direction. But it's failure also succeeded in motivating a number of biologists to continue to pursue group selection research. And from the point of view of relative significance frameworks, this episode fits really well when Edwards conception of group selection was not successful in the 19 sixties and seventies. And in fact, as a result of the response, it stimulated lots of work at the individual level. But the Group Selection debate is one that appears to be continuing into the present. And in this contest, like a diametric can't contests in this context. A diametric contexts between group or individual as the unit of selection is subsumed into a hierarchy of multilevel selection theory that acknowledges the action of selection at multiple levels. So natural selection is not just working on genes, not just working on traits. It's not just working on organisms, it's working on multiple levels. And this complicates Darwin theory, complicates Darwin's theory, but it also compliments Darwin's theory. It connects to the original ideas and sort of take some of the new stuff on board. And I think again, this is the value of looking at these debates. This is the nature of the scientific process. There. There are, there are always kind of new ideas and those need to be incorporated and considered. So I'll clue, I'll close with Gould again with just a line from, I think this is like page 1335 or something like that, to ridiculous tone structure of evolutionary theory. But he writes, natural historians have too often been apologetic, but most emphatically should not be in supporting a plurality of legitimate scientific modes, including a narrative or historical style that explicitly links the explanation of outcomes not only to the spatial, temporarily invariant laws of nature, but also if not primarily to the specific contingencies of anti antecedent states, which if constituted differently, could not have generated the observed result. Gould here is referring to sort of phylogenetic history and phylogenetic Lindsay lineages. But I think we should be thinking about history of science here to these two debates over punctuated equilibria or tempo and the level of selection, I'll call that mode for, for, for lack of a better phrase, demonstrate that science is a process that is done by invariably fallible humans. And that looking at the details of controversy in science, which arises whenever there are new ideas can help students understand that science doesn't represent a long list of facts or answers. Rather, it gives us an opportunity for understanding and asking further questions. So thank you. I think I went over well, thanks so much Mark, to incredible kind of controversies. And this has been a great introduction and so delighted to see you picking up on Steve gold as well. Is there a question from the audience, please? John? This is how light? One of the things I've never had a real problem with punctuated equilibrium versus gradualism. It seems to me that we have this concept of molecular clock, which is sort of the gradualism kind of issue where it deals with many genes. Whereas we talk about punctuated equilibrium, we're looking at morphology which could be influenced by just a few genes. And therefore, really, what is it we're defining as evolution as a process? Or is the morphology? And is there really a controversy here? I'm just being naive. Should I respond to that? Yes, please. Yeah. Thanks for the question. I mean, it's super interesting and I don't think that you are being naive. I think it sort of points to one the ways that controversies turn into these kind of binaries where it's like, oh, either it's this or that. And I think that, you know, right? So if you're looking at the genetic level and you're thinking about cameras neutral evolution. And, and, and you feel like, well there's a lot that happens, that means nothing. And they're at the genetic level or that isn't seen by evolution. And there may be massive morphological changes that are the result of a very small, are few in number genetic changes. Which is right, or which is more important. And I think, you know, my answer and I think it's consistent with all dancer in some sense. Is that well, it depends. Right? I mean, it depends on what lineage you're looking at. It depends on what period of the phylogenetic history you're looking at. And it depends on sort of, you know, yet well, so it depends on the context, right? So this is the other thing, it's stasis is data, context is content. So, so what you need to have in mind when you're, when you're doing your evolutionary analyses. Is this kind of multifaceted, multifactorial kind of analysis. Not sort of the, the kind of either or either. It's something that is sort of the, the gradual mystic molecular clock, neutral theory kind of thing for it's like massive morphological changes at the organism or the lineage level. They're constantly kind of interplay of, of all of these 2 plus all of the other things that are affecting evolutionary trajectories. That does, that makes sense. But it's just that it seems to me that there's, I mean, there's Allen Wilson did some work and he showed that, say, frogs, change in morphology very little over time, but the rate of evolution of the molecules, the total organism, was fairly constant over time and not particularly different from say, mammals, right? So what is the one thing? Again, this may say something about the level at which selection is acting. So, so, so folks who weren't particularly sympathetic to two, to Dawkins, you know, everything of significance is happening at the genetic level. Would say like, well, it may not be that significant genetic change that we need to be tracking. We should be looking at the, there may be plasticity, there may be other kind of, there may be epigenetic effects. There may be all these other kinds of things that would account for these kind of morphological changes that aren't represented by any significant genetic change. The track. There's a question from John, have hashrate or speak. I refuse to take questions from John. Well, Mark is kind of weird circumstances because I'm taking my setup for firms ski club and he just got the car, so all right. Bye. I want I wanted to ask you about something now because when you were talking about the relationship between Meyer as if I let a gradualist and gold and Eldridge, but they're punctuated equilibrium. You know, you know this, but a lot of other people might not, that there's a little bit of a weird conceptual relationship there because to some degree you could, you. Golden Eldridge is punctuated equilibrium as an application of an idea of Myers, which was allopatric speciation. But that allow the evolution might be taking place like off to the side, right? You know, um, other area that, that knows how it's evolved, individuals move in and in the fossil record it looks like they suddenly replaced. Yeah, was there or in the area where the fossilization has taken place. And so the only reason I bring that up is because I think if you made a real like a really cool point that you bet, it's the idea that a lot of these ideas from evolution really apply to conceptual evolution too. And so here you have this idea of goal, or sorry, of Meier, who looks like he might be completely like have a completely different view of evolution and cool. But really what As you sort of repurposed a module in the same way, a lot of times happens in evolution where it gets co-opted for some new purpose. Nice. Yeah, yeah. There's there's really a lot more to be. There's a lot more to your story about how evolution is helpful in understanding the history of science. And I think you're, I think at why I totally appreciate that. I'm not going to take it as a question, I'm going to take it as a comment. And I'm going to say, thanks for thinking that was interesting. And I think, I mean, obviously, I'm not surprisingly, I think you're right. But I'll I'll I'll I'll I'll I'll I'll make a comment on your talk tomorrow night. I gotta take you right to left the letter. H, John. Thanks, Mark. I'm going to answer one question in the question answer aquatics by Andrea Anderson is just an ongoing debate on the speed of Evolutionary Theory been widely accepted in paleobiology. I would argue that the debate continues to go on and I think Mark agree how to tell it? Kind of, yeah, yeah, Thanks, Julia. And I think the power of controversy and she is really important here. And so thank you so much, Mark. I really appreciate it. Thanks again. I'm going to turn it over to QC. The entropy. The other talks you here. Thank you for doing this. Good evening. Thank you so much. And I think it's, it's really especially important these days to talk about the nature of science and for obvious reasons, thing won't go into. But I just wanted to mention that our last speaker this evening is Dr. David Fanning, who is a professor of biology at the University of North Carolina in Chapel Hill. And he's the 2020 one of the 2021, 2020 to sickness I distinguished lecturers. I'm so he often gives talks to general audiences like this one. His work has been funded by National Science Foundation. He's a contributing author to Scientific American that's been involved in a bunch of television series and National Geographic shows. And we're very, very happy to have him here to speak to us today. So I'm his talk is entitled plasticity, epigenetics, and evolution. So thank you, Dr. Friend Nick. Well, thank you. Thank you, Karen for that. Nice introduction and thank you, John and Karen for inviting me to be here tonight. Thank you for the organizers is this is terrific that you guys have this have this program. I'm Thank you guys also, if everybody for coming tonight and I'm sorry, we can't be in person together, but I think unfortunately, maybe unfortunately we're all getting used to Zoom now. So what I'm going to talk to you about tonight is I want to talk about plasticity, epigenetics, and evolution. And I'm going to define what I mean by these terms here in just a moment. But of course we're here tonight to celebrate the birthday of Charles Darwin and so on. Well, let's just begin my talk by asking, what is it about Darwin? What did you discover that we still celebrate even today? And so Darwin's great discovery, eras grand theory really was this idea of evolution by natural selection that I'm sure you're all aware of. We've already heard a little bit about tonight. But the reason this idea is so important is because it explains this, that is, that explains the diversity of the natural world. It also explains why living things tend to be so complex. But it also explains why living things tend to acquire features that enabled him to survive and reproduce in their environment a little bit better. That is, it explains adaptation. So it's worth just stepping back for a moment and ask you, well, how does this process really work? And we already got it, sir, preview from this endeavors taught, but we just want to emphasize a little bit more than one of the things that was so brilliant about Darwin's idea of evolution by natural selection is that it's such a simple idea. And what Darwin said is that evolution by natural selection will occur when you have just three conditions, they're satisfied and natural population. And the first of these conditions is that you have to have variation. So individuals have to differ in their traits. So in this hypothetical example, we've got these bugs and he got some red bugs here and some green bugs. Secondly, he said You've got to have differential survival. Reproduction that is summative is how does survive a little better than others or reproduce little bit more than others because of their distinctive features. And so here you see the green bugs being eaten by the birds and then the red bugs or are being favored in this case. And then thirdly, he said you had to have some mechanism of inheritance whereby individuals transmit the next generation, those favorite features. So if you have these three condition is met, then you're guaranteed to get evolution by natural selection. And again, that's why this idea is so powerful and why it's, it's, it's, it's, it's still relevant even today. Now, if we look at these different conditions a little bit more detail. The one that Darwin really struggled with the most, the second one, differential survival and reproduction. And yeah, this is probably the most intuitive all these conditions and it's the one that you can go out in nature now and you can look at organisms and see some survival are better than others or reproduce better than others. And indeed, Darwin did this themselves. In contrast, Darwin was really puzzled by what causes variation and inheritance. And one of the sort of themes of my talk tonight is going to be that although we tend to think that we've solve this problem and understanding variation inheritance. I would argue that this is still even today, a little bit of a puzzle for us. And what Darwin's Dilemma was was to explain the causes of variation and inheritance. And in his big book on the Origin of Species, which he published in 1859, he says, Our ignorance of the laws are, our ignorance of the laws of variation is profound. Not in one case out of a 100, can we pretend to sign any reason why this or that part has varied as it has. And then he goes on to say, I think there can be no doubt that increase use a certain parts or a domestic animals has strengthen, enlarge them and disuse diminished in and that such modifications have been inherited. So this idea that Darwin had, that variation is caused by use or disuse of structures as organisms that live in their environment. And his ideas on inheritance that once individuals acquire these features, they can pass them on to the next generation is probably very unfamiliar to many of you. And so one of the things I want to explore today is like worried Darwin cope with these ideas. And was he completely wrong, or is there some truth in what he's saying here? And so there are three key questions that I want to focus on in my talk tonight. And these are really sort of the, the outline of my presentation. The first question that we're going to ask is, was Darwin right? Can the environment influence the features that an organism produces? And just to give you the punchline upfront, we're going to see that the environment can in fact profoundly affect trait variation in many organisms. Given that the environment can influence the features that an organism produces. Then the second question we would ask is, can environmentally influenced features that an individual acquires during his lifetime? Can those actually passed on to its offspring? And again, we're going to see that some environmental influence features can actually be passed to offspring. And then thirdly, we're going to ask sort of big picture question about what role do these do these sort of environmentally influenced features play and evolution. And we're going to ask an environmental influence change actually impact a species evolution. And again, the punchline here is we're going to see that environmentally influenced change might actually jump start evolution and indeed might play a critical role and promoting or facilitating evolution. So before I get into these questions and answers these questions, I wanted to step back for a moment and I'm going to spend about five or so minutes talking about sort of how did we get to today in terms of our views on variation inheritance. So, sorry, keeping with, with Mark's talk, I'm going to discuss a little bit of history here. So this is a brief history on ideas on variation, inheritance and our story. For our purposes tonight begins with two scholars, Erasmus Darwin and Giambattista Lamarck. And you can see they lived in the latter part of the 18th century and the early part of the 19th century. Now if Erasmus Darwin's name sounds familiar to you, it should be because in fact, this is Charles Darwin's grandfather. And 1 I wanna make here is that Darwin didn't invent the idea of evolution is grandfather actually had published a book on evolution. But Erasmus, Darwin and Lamarck both argued that in terms of where variation came from, that a lot of variation was caused by the organism is interacting with their environment to this or use and disuse that, that Darwin discussed. And Lamarck is doing this most famously associated these ideas. We're going to focus on his ideas here primarily. And one of the classic examples was that of the giraffe. And he asked, Well, where did this distinctive feature of the draft come from? The long neck. And what Lamarck suggested was that drafts develop their long neck during their lifetimes, from the constant stretching to get to the upper parts of the trees. But then he further said that once these traits were acquired by an individual during its lifetime, then they could pass those features onto their offspring, their offspring that would be born with a slightly longer neck. Now this process that Lamarck is discussing here is sometimes referred to as the inheritance of acquired characteristics. Now it's easy to sort of poke fun at this idea, but it's really, it followed naturally from the observation that we can make even today, that certain features change with use or disuse. So for instance, if you think about a blacksmith as they use their arm or they will develop the muscles that arm. To a greater extent, but also the unmarked discussed organisms like moles that burrow into the ground and I don't need the eyes. And he knew that they were born blind. They're born without eyes. And so he suggested that this was because of the disuse of not using those eyes. They've lost that. But the other basis of this idea, the inheritance of acquired characteristics, was the widespread belief at the time that most reproduction are really all reproduction is merely a budding process. So when you look at organisms like brewer's yeast or hydra, see here is that the offspring essentially but off of the pair. And if that's the way reproduction works and you can easily see how traits that individual cars and its lifetime are going to be automatically passed its offspring. And even in humans, people thought that there was sort of a budding process that reproduction entailed. And at the time people believed in something known as the modulus, which was that there was a tiny human inside the head of the sperm. And that reproduction simply involve the unfolding of this little him and during its, during its early development. Now, why do people no longer sort of adhere to this idea that hurt us acquire characters and the person that's sort of given credit, if you will, for disproving this idea, is the German embryologist August Weissman. Now Wiseman was an early, very important proponent of Darwin's theory of evolution by natural selection. And he was really important in advocating those ideas in Germany. But towards the end of his life, Vice me became very puzzled by the problem of where new traits come from, how variation arises. But he also was really puzzled with how inheritance worked. And one of the experiments that he did was he took mice and he cut the tails off these mice and then he measured the tail length of the offspring. And you repeated this process for five generations. And when he wrote was that 901 young reproduced by five generations of artificially mutilated parents. And yet there was not a single example of a rudimentary tails that probably doesn't surprise any of you that didn't find a mouse born through marry til. So he took these kinds of experiments, but he also took a number of observations that he made of how embryos developed. And he came up with an idea of how he thought development work. And this idea which is still with us today, basically argued that organisms, multicellular organisms consists of two different types of cells. First of all, there's what are called the somatic cells or the soma. And these are the cells of the body that you see. It's the muscles as the eyes, the skin and so forth. But he also said there was a special set of cells often sequester deep inside the organism that he called the germline or the germplasm. Now, he suggested that as the germplasm that's actually perpetuated across the generations. And that within each generation than the germplasm through development gives rise to the soma. But importantly, what Vice been argued is that the sum of one generation and could not directly influence to some of the next generation. But also he suggested that the soma of the one generation couldn't also influence the germline of the next, that's going to form the next generation. And so this is sometimes referred to as vitamins barrier. That there's a barrier between what happens in one generation and what happens in the next generation. And so this was his idea of how you could not have the inheritance of acquired characters. Now, Weisman knew there was something, again, a special set of cells that he called the germplasm, but he did not know what that germplasm consisted of. But while vitamin was developed easy developing these ideas 1980s. There had been a scientist or scholar who decades earlier had discovered indeed what that germplasm consisted of. And this person was the aforementioned Gregor Mendel, which we already heard about tonight. Now Mendel was it obscure monk who lived in what is the modern-day Czech Republic. And he conducted a series of experiments with pea plants where he bred peas that had different characteristics. And from his careful experiments, what he deduced was that parents pass their offspring discreet invisible factors would predictably influence the traits to their offspring. Now he published this work in 1865. So this is only six years after Darwin published his big book. For reasons that are not clear to many. I think these ideas were largely ignored. And in fact, it wasn't until around 1900 when three scientists, within a span of only three months independently recapitulate or rediscovered Mendel's work. And once the, his work was rediscovered, then these factors that Mendel described, referred to as genes. Now the other important discovery to our story tonight was. Understanding what genes consisted of. And this discovery was made in 1953 with the discovery of the structure of DNA. And this work was conducted by James Watson and Francis Crick, using the work that was also conducted by Roslyn Franklin. Unfortunately, she wasn't able to share in the Nobel Prize with them because she had been deceased. But what they discovered is that DNA, which again is the chemical that makes up genes, consists of this double helix, the source spiral staircase that you're all probably familiar with. But importantly, what they found is in the middle of that spiral staircase along the rungs are these four chemical bases. Adenine, thymine, guanine, and cytosine, abbreviated as a, T, G and C. But they found that a and T always linked up to form around and G and C always linked up to form wrong. And that's going to become important here in just a moment. But following their discovery and then work that a lot of people had died over the next few decades, we began to understand how the information encoded by the sequence of those bases in the DNA then is translated into the proteins, the amino acids and proteins that make up living organisms. And one of the things that came out of this work though, is that, that sequence actually matters greatly to sequence those bases. Because in this case, if you change one litre there, that a to a T, you get a new amino acid. It goes from glutamine to veiling. And that when change in humans will cause the carrier then to develop signaling and the red blood cells and will lead to sickle cell anemia. So discoveries like this then began to suggest that people that DNA now was the missing link for explaining trade variation. And going back to solving Darwin's Dilemma. But also people began to suggest that DNA was the missing link for explaining inheritance. Because when, when researchers understood how DNA replicated, it became clear how it was that parents and offspring tend to resemble each other, pick or during reproduction. When DNA is replicated, then the, the helix unwinds at each of those individual strands, then serves as a template for the new strand. And so remember we said that a and T always bind together and G and C. So you end up with two daughter molecules that, that maybe we'd been say the sperm and egg that are identical by an occasional mutation to the parent molecule. And again, this could explain why baby giraffes look like their parent graphs. Not because they are part of those traits during your lifetime, but instead because they acquired that DNA. So this is the world we live in now today, we live in this sort of gene centric and DNA centric world. And if you were to go right now onto the NIH's National Human Genome Research Institute's web page. And you'll see this page that says, what's a genome that opens up? And it says genome is a fancy word for all your DNA. And then I've highlighted the key phrase here. It says, each genome contains the information needed to build and maintain that, that organism throughout its life. So we live in a world now where we basically teach our students, who teach the lay public, that everything is about DNA and about genes. But here's the problem, and this is going to get us into the three questions I raised the outset. This gene centric view is correct than how can individuals with identical DNA produce dramatically different traits? And let me give an example. This, so this is a wonderfully, this is a small crustacean, barely visible to the naked eye. They're found in freshwater worldwide. Now these are really small little things. And like a lot of small things, everything tries to eat them up and they kind of trick up their sleeve. And that is that if they experience predators and their water, then these individuals will begin to develop a completely different form like you see there on the right. And in particular you can see they begin to produce this helmet on top of their head. And we're going to see in a moment that helmet actually makes them a little bit less susceptible to predation. But the important point here is that these guys actually reproduce clonally. So you can take a single clone of individuals and not exposed to predators and you'll get that normal form the sum the top there on the, on the right top. But you expose other from that same clone to predators and you get this hominid form. So you're getting very different traits being produced missing or genome identical DNA and source are standard view of how traits generated then doesn't seem to hold in this particular example. But another thing that we can't explain with a certain gene centric perspective is certain perplexing patterns of inheritance. And in particular, sticking with these water fleas, once individuals produce that helmeted form, then there's a good chance that their offspring will be born with a home AT, even though the offspring themselves did not experience the chemical cues from the predators. Now you're probably thinking, well maybe there's something weird about these silly little water fleas define anything like this and other organisms? Well, the answer is you find these kinds of patterns and all kinds of organisms, including even humans. And let me explain one example here from humans. Well, a recent study, analyze harvest records from a town in Northern Sweden. You can see from 874, 910. And what the researchers found was there was a strong association between food availability in one generation and disease and later generations. And in particular, researchers found that the amount of food a grandfather had II, between the ages of nine and 12 was especially important. Now that age, that window of time nine to 12, age when boys form the cells that will produce sperm. And so what the researchers discovered is that if that boy had intermediate or poor access to food when he was nine and 12 years old, then his grandson's had normal health. But if his boy had high access to food during that time window, then his grandsons were more likely to die of cancer. Now this was not an effect seen and the females, and it wasn't anything seen in the sides, it was only detected in the grandsons, but it's a highly statistically significant effect. And so it suggests there's something being passed down to the grand sons that can't be explained through sort of a normal way of looking at how inheritance works through the transmission of DNA sequence changes. So in light of these perplexing patterns that we had to explain, let's come back to these three key questions that have caused the outset and let's begin with this question. Can the environment influences the features an organism produces? What we now know that the environment is actually crucial for normal development. And indeed, all traits or phenotypes emerged during development from an interplay between the organism's genome and it's an environment. And let me just give you one example. This, so this example or from mice. And what you see here are pictures of mouse guts. And the green color here is highlighting the gut capillary network and the mouse's intestines. The left there you can see a picture of mice when they're reared in a germ-free environment. Now, you probably don't see this, but you can see from this is that bat capillary network is very poorly developed and indeed these mice have very poor health. On the right though, is a picture of the gut Capra, the network of the same mice, but now ten days after they were inoculated with normal gut bacteria. And now you can see the intestine, the gut capillary network is developing much better. The mice are much healthier. So in this case, the environmental change is the, is the presence of these bacteria. Now, this sort of capacity for is, is there respond to changes in the environment is widespread. And indeed I would suggest it's a defining feature of living things. And this phenomenon is what we referred to as phenotypic plasticity or simply plasticity. Now the existence of phenotypic plasticity then gives rise to flexible organisms. And let me just give you three more examples of this. So on the left are two different leads you can see from the same plant. And what happens here is that these plants, these certain aquatic plants, will produce that sort of thin leaves. A sound left there if they grow under water. On the same plant, the leaves that grow above water develop into the sort of broader form. These two on the right there, in the middle are different castes have asked, and as Debra mentioned earlier, and ants, bees and lost and termites, they produce these different castes. And in many species, whether an individual becomes one cast or the other, in this case, what's called a major worker or minor worker. These leafcutter asked, is strongly influenced by their diet early in life. And then on the right or to Brock cartograms. And these are, you can see different color morphs, different seasonal forms here. And many mammals, birds and insects will produce different color morphs. In this case, they're paying upon day length. Now, plasticity, It's important to think about why it's why this phenomenon is so widespread. And 1 I wanna make about plasticity is that unlike evolution, plasticity can generate change within a single generation. So for instance, on the lower left there is a familiar example of plasticity. This is a plastic response and Venus flytrap, where in this case the leaves will close within 40 milliseconds of an insect touching the trigger hairs there, so it's very, very rapid. Now evolution can sometimes occur very rapidly. On the lower right is a classic example of very rapid evolution. And Galapagos Islands, medium ground finches, where you saw a shift across just two generations, one generation to the next. But nevertheless, evolution by definition has to occur across generations. It can't occur within generations like plasticity. But another important point about plasticity is that it's often beneficial. So as we saw in the water fleas earlier, we noted that they produce, that's how many form in the presence of predators? Well, if you look at the survival of these two different forms in the presence of predators. You find that they have much higher survival if they produce that helmet and form that if they produce the normal form of the left there. And the reason should be very obvious to you, which is that the helmeted form basically makes the wonderfully larger. And the predators here are what are referred to as gape limited. So they can't, if somebody gets too big, they can no longer eat them. Now that's important because, you know, plasticity provides a mechanism where whereas, where organisms can respond by producing an appropriate trait for current conditions in their environment. And that's a contrast to genetic mutations. Because with a genetic mutation, the chance that a particular mutation will occur is not influenced by whether or not the organism is in an environment in which that particular mutation would be advantageous. Now, Plessy, putting this all together, we think it enhances fitness in a variable world, all organisms experience variation their environment and maybe seasonal variation. It may be daily variation, it can be longer-term variation, but all organisms are experience, the experience variation. In Placitas, he provides a mechanism whereby organisms consensually match traits, their phenotypes, to the current conditions that they're experiencing. And so they took him can minimize that mismatch that can often arise between organism's traits and its environment. And so let me just show you this in sort of a cartoon fashion. So let's imagine we have three different genotypes are three different genetic compositions of these lizards and a population. We have a lizard that has a genotype, that means it's dark all the time. It's fixed for being dark. We have a genotype that mean just like all the time, It's fixer being white. Or on the lower right, we have a genotype is plastic, can be dark or light depending upon its environment. Now let's further imagine that these lizards experienced two different kinds of environments. They experience a dark environment or light environment at different times their lives. Well, if you look at the fitness of the dark lizard, you would expect that the course have highest fitness in a dark environment where sort of blends in the lowest fitness on the light environment. And then you would expect the opposite for the light lizard, the light fixed lizard genotypes. So highest fitness and the light environment, lowest fitness in a dark environment. So you can average those two fitnesses across both those two different forms because they're going to experience both environments over their lifetime and you get some value. It's indicated thereby the horizontal dashed line. Now let's go to the right and let's look at our plastic genotype. So we can assume maybe there's some cost of plasticity. So it's kind of a little bit lower fitness, either the dark or light environment than the dark or light fixed form for which those are two specialized for. But overall, the plastic genotype is going to have higher fitness and you're going to get this increased fitness of the plastic genotype as you've averaged across all these environments is for this reason that we think plasticity is so widespread. Now you might be asking, well, how does plasticity work? How do we think this process works? And so our modern understanding of how of molecular biology and one model for how plasticity work as works is as follows. So the idea is that an environmental change causes signals to be conveyed inside the cell. And so those signals are conveyed into the nucleus of the cell where the chromosomes reside. And the chromosomes are, where are our consists of the DNA. Now, once those environmental signals get down into the nucleus and interact with the DNA, this can cause proteins to bind to specific DNA sequences. Now it's the binding of those proteins, those sequences, they can in turn activate a nearby gene and then ultimately cause the trait to be produced. So it's almost like an on-off switch gear that you have. If the signal is there and those proteins bind to the DNA, the signal is the switches turned on. If they're not there, it's like this which has been turned off. But here's the key point. Because different environments produce different signals, and because different signals activate different genes, different traits, they can be produced from the exact same genome. Now another way in which plasticity can work, though, is when an environmental stimulus causes a small chemical group, what's called a metal tagged as simply a carbon with three hydrogens to be added to the DNA strand. And specifically to be, to, to link up to the cytosine on DNA. This addition of this metal tag can influence gene expression. And so again, it's like an on-off switch. If you've got a lot of these methyl groups added the DNA, then it's like the DNA, the genes along that stretch of the DNA turn off. If you've got very few of these methyl tags added, then it's like the, the genes along that stretch of the DNA being turned on because the DNA's relax and coiled and then the chemicals that cause the genes to be turned on and to read those genes then can access the DNA in that case. Now, let me give you an example of this. These are mice that are genetically identical each other. They differ only in their DNA methylation patterns and those caused the kink in the tail of one mouse but not the other. But also experiments have shown that the effects, these tags on trade production, can be actually demonstrated through sort of a cause and effect. Let me explain what I mean by this. So people who study rats and mice have long known that if a mouse is a baby mouse or rat is grown up with an anxious, non nurturing parent, mother, it will self-growth and are not anxious adult. In contrast, if that pup is raised by a relaxed, high nurturing mother. Will become relaxed adult. Now people began to suspect that these differences were caused by methyl tags being edited or DNA. And so when researchers were able to do is to take a drug that adds these methyl tags to the, to, to the rat and inject it any relaxed, high nurtured rat. And they can basically convert that rat and an anxious rat now to the most important environmental causes of methylation or diet and stress. And so this is why diet and stress early in life can have really long-lasting effects and why we need to be mindful of these sorts of facts. Now, these sorts of mechanisms that create phenotypic variation without altering DNA base pair sequence. There were called epigenetic beyond genetics. So you've seen an example of a genetic mutation, the sickle-cell anemia, where one of those base pairs, base chemical bases, one of those letters got changed. But now we have an EPI genetic mutation where as you add the methyl groups today, it can lead to dramatic, in some cases, dramatic changes in the phenotype, such as you see in the mice in the lower right. So what we've seen here is that in response to our first question, the environment can indeed profoundly affect trade production via plasticity, an epigenetic changes. So given that, we now want to turn to our second question and ask, Can these environmentally influenced features be passed to offspring? Well, we already know that the answer to that question is yes. We've already seen a couple of examples from the water fleas and the sweetest grandfather's where environmental changes were inherited by subsequent generations. Now I'll just say up front, we don't know for sure what the mechanism is in either these two specific cases, we have some hints of what might be going on here. But what I want to do is I want to suggest one possible way in which our mechanism that could lead to these changes. So recall that an environmental stimulus can cause a metal tagged to be added to DNA and then that affects gene expression and that could change the traits that are produced. Well, it turns out that during reproduction, during DNA replication there are special enzymes that can copy these methyl tags from parent to daughter strand. And then that will cause the offspring inherit the altered gene expression patterns and ultimately to produce the trait that is influenced by those methyl tags. So in this way, environmentally induced changes can in fact be inherited. Now, people have studied this quite a bit in the case of understanding cellular differentiation and knowing understanding that epigenetic inheritance is what underlies the fact that the different cells, any multicellular organisms, body differentiate and these different cell types. All right, So in our body we start out with stem cells. And you'd gotten our bone cells and fat cells and muscle cells and so forth. But also epigenetic inheritance can underlie the cell inheritance here because once you have bone cells differentiating, those bone cells give rise to another generation or bone cells, which makes sense because it would be bad for them to suddenly give rise to say a neuron or muscle cells or whatever. So we've long known that epigenetic inheritance can underlie inheritance at this sort of level within the bodies organisms, the question is, can these effects actually be transmitted across generations of individual organisms? Well, this has been a controversial topic, but there have been studies now for almost two decades showing priest convincing evidence that these effects can in fact be transmitted across generations. And one of the earliest studies that show this found that if you take pregnant rats and expose them to pesticides, then their signs, their grandsons and they're great gatt grandsons suffered poor health and reduced fertility. And this study also found altered DNA methylation and the sperm suggesting that it was indeed these methylation patterns that were causing these effects. Now I want to just emphasize here though, that transgenerational epigenetic inheritance, what we're going to call transgenerational epigentic hertz. It can mean it be mediated by mechanisms other than through the transmission of methyl marks, such as we've seen in a really remarkable study came out a couple of years ago, showing that in mice express dependent RNA. Remember this the other chemical related DNA, it's the single-stranded sort of cousin of DNA. It can be transported from the brain, whereas initially expressed to the germ line, those germ cells of mice and ultimately to the offspring. And so the bottom line here is that parents can transmit numerous factors their offspring, other than genes that can influence the traits their offspring. They can transmit. Metal tags will be seen. Rnas we just saw. But of course, nutrients and metabolize hormones and proteins and especially things like mammals where they, they have intimate connection with their offspring, would think that parents can also transmit microbes their offspring that can dramatically alter the traits those offspring. And so you see this pill bug in the lower right. And in pill bugs. Parents can transmitted Bactrim to their offspring that can actually change the sex of their offspring. And so this is a dramatically influencing the features. They're all of the offspring. And it's not the transmission of DNA. Base pair sequence changes as these other materials that are being passed down. So in response to our second question, we've seen that indeed some environmental influence features can be passed to offspring via transgenerational epigenetic inheritance. And so we want to stop teaching our students that, you know, this can't work because there are clearly examples where you can in fact have environment influence features that are required during their lifetime that can be passed to offspring. So last question I'll focus in on is the one that I spend most of my own research studying, which is this question of can environmentally induced change actually impact of species evolution? Now, this, this problem of the relationship between plasticity and evolution goes way, way back. It goes back before Darwin to people like we saw Lamarck and an Erasmus Darwin. And it's really been puzzling people for a long time. And I think if you were to ask most evolutionary biologists even a day, what role plasticity plays an evolution? You'd probably get an answer somewhere along the lines of the following. In this quote is from Ernst Meyer, who we heard about from Mark, is one of our leading evolutionists of last century. And we'll talk to you about classes that he's impacts on evolution. Meyer said the ability of the phenotype to respond to the demands the environment without mutation that so it's a long way of saying the ability to express plasticity, he says, greatly reduces selection pressure. As the idea here is that if you've got the ability to express different traits in response to different environments through plasticity. That's going to basically dampens selection for diversifying evolution. And so essentially what he's saying here is that plasticity, if anything, we should slow evolution down. Now posing this view as an alternative view that's also been around for a long time. Which suggests that rather than slowing evolution down, plasticity may speed it up. And I think this view is most, most accurately captured by this quote from the evolutionary biologist mary jane West. They were hard. He published a very influential book in 2003. And in this book she said most phenotypic evolution begins with environmental initiate change. So she's saying most of you took evolution actually begins with plasticity. And then she goes on to say genes are followers, not necessarily leaders and phenotypic evolution. So again, she's suggesting that plasticity, rather than slowing evolution down should speed. So how would that process work? Well, I'm going to just outline here an idea that we've dubbed the plasticity lead Evolution Hypothesis. And I'm going to illustrate this hypothesis with a series of cartoons. And what do you see here on the panel a is you see a genetically diverse population, this case these are tadpoles because that's what I study. Now, notice that these tadpoles all the same size, they're all the same shape. So that's meant to indicate initially they had the exact same traits are the same phenotypes. The different colors are actually meant to signify different genotypes are different genetic compositions of these different tadpoles. Now in panel B, let's imagine the environment changes and as we said, are that's going to happen to all organisms at some point, if not in our lifetime, certainly in their evolutionary history. Now I'll change the environment is typically stressful to all organisms. And the main way that organisms deal with the stress associated with a change in their environment is to use their inherent plasticity to produce new phenotypes. And so what you can see here is that these tadpoles are now different shapes. You notice the blue genotype has become a sort of fat bodied form. The maroon colored one is becoming a skinnier farm and then the green is in-between those two. Those are all outlined in white here. But then the orange one, which is not a line and y is not changing at all. Indeed, this raises a really important point here, which is that plasticity should not be thought of as non-genetic change. Because in all natural populations where this has been studied, we find there's underlying genetic variation among different genotypes and whether, and how they will respond any particular change in the environment. So once that variation, that formerly cryptic jagged variation is revealed, a selection in panel C selection can start to act on that variation. And so let's imagine that the fat body form is now the favorite form in this new environment for whatever reason, selection favors that form. It disfavors the other forums and hence a disfavors the underlying genotypes that influenced those other forums. And over time in panel D, you get, you can actually get adaptive refinement of that forams. You get enlargement of that form shown in this picture. Now eventually one outcome of this process in panel E might be too, where you get different phenotypes being produced in different environments through plasticity. And this is a process known as polythene ASM. But another possible outcome is that you might actually lose the plasticity and hours. The population might go towards fixation. But in this case, fixation of this new The stat bodied form. And if that happens, yellow process that was dub, genetic assimilation. But the important point here is that regardless of whether the end result of this process is a polytheism or a new fixed trait. Your genetic simulation, you're getting novel trait being produced by this process. And it wasn't a new genetic mutation that caused this novelty to combat. Instead, it was the plasticity that revealed and align jagged variation to selection that got this whole process rolling. And that's why mary jane less Eberhard refers to genes being followers, not to say leaders and adaptive evolution because they're just sort of falling along. So the question is, how do you test this idea? Well, one key point here is that you can see there's subtle. You would predict that there should be subtle genetically variable plasticity in some ancestral lineage of some organism that you might be interested in studying has some novel trait. But the other key feature, this is that that preexisting plasticity is going to undergo adaptive evolution and in derive lineages, why do you get a polytheism or you get genetic assimilation? So we've been testing these ideas and a remarkable group of amphibians known as spade foot toads. And this is showing you the seven recognize speech, the state foot's in the US. You can see they're found from coast to coast and from Canada and Mexico. But you can also see there Sarah, origin is down in the Southwest and New Mexico and surrounding states. And indeed, These guys are among the few amphibians that have successfully invaded the, the warmest, driest parts of our continent. And here we're looking at a small pond from this past summer. Those are my two teenage daughters standing next to a new Mexico and this is a typical state that breeding pond. Now if you go into these times and if you look at their tadpoles, you find something really remarkable. So many there tadpoles looked like perform that you see here, which is a typical looking tackle that you've seen where in the world. But you find that if they eat meat such as these fairy shrimp, which are found in the same pons with them. Some of those individuals through plasticity will produce that's very distinctive form the sound the right here. Now we refer to these as the omnivore on the left and the car will morph on the right. And they differ in important, a number of important aspects including their total debt length. And so the omnivores, you might not be surprised, develop really long gut. Whereas the carnivores that you can see there on the right develop a really short gut. So what we wanted to know is where did this carnival morph come from? Did this carnival morph evolved through sort of plasticity, let evolution process. So we begin by looking at a species in a genus SPIA and we find they express this enhance plasticity if you feed or if you feed different individuals from the same families, Anita plants or shrimp, the ones that are fed on plants, boys develop really long guts and they develop that omnivore form. If you feed their brothers and sisters on shrimp, they will develop shortcuts and develop that carnivore morphs. So they have this polytheism. Now if we work our way backwards though, when we look at a species that concern represent the SAR ancestral condition here, we find that they don't express that car were morph, but instead they've got subtle plasticity, but it's also genetically variable. And so you can see they start producing slightly shorter guts on the shrimp, then on the plants. And those different lines are signifying the data for different genotypes. And that's exactly what we predicted. And the, and the Pleistocene let evolution started outlined earlier. But also we're going the other direction. Certain lineages and this species SPI Obama fronds that appeared have undergone genetic assimilation. They've lost the plasticity regardless of whether you feed them on plants or shrimp, they always dealt the short guided carnivore morph. So we think what we're seeing here is that you're seeing different stages, this evolutionary process. In other words, we think we see the sort of subtle plasticity started off than the polythene is a vase. And now finally, fixation of a novel form among all these three living species. So as we think we have evidence for class to see what evolution. And this isn't the only system where this has been found. We now have increasing evidence and dozens of examples from nitrogen-fixing cells and cyanobacteria to cast and social insects, the rattle, rattle snakes. And even I loss and cave fish that appears to have evolved through this process of plasticity let evolution. So in response to our third and final question, and we've seen that environmentally influenced change might actually jumpstart evolution. And it might actually, the sort of plasticity might play a really critical role and instigating and actually facilitating evolution. And so we need to think more broadly about this process and not simply that it's an impediment to evolution. So I just want to close a file. General thoughts. 1 I wanna make is that studies of plasticity and epigenetics demonstrate the trait variation and inheritance involve more than just genes. We seen that most traits, indeed I would argue all traits emerged from an interaction or an interplay between genes and the environment. And so in a sense, Darwin was really right about this. But we've also seen that these studies reveal that what happens during our lifetimes can influence the health of future generations. And so it's not just about, oh, I'm going to transmit good genes to my descendants or bad James, my distance or whatever it is, it's what you're doing in your lifetime. They can actually cause changes to occur to your genome. You can pass on to future generations, so you have some control over this. And that leads to my third and final point that these studies suggest that chance may actually be less critical in both evolution and human health and is often assumed. And so evolution we tend to teach our students that, you know, it's all driven by random mutations that selection is acting on, that may not always be the case. And even in human health, we say that this person has this disease or not. It's just bad luck or good luck. And again, it may have more to do with with how individuals actually live there, their lives. But I wanted to skip the last words here to our birthday boy Charles Darwin. And at the very end of his life in 1882, when he passed away, he was asked by August of Iceman to write a preface for one of vitamins books on the causes of variation inheritance. And I want to just read some keywords from that process because I think they're very poignant. Darwin said, several distinguished naturalists maintain with much confidence that organic beings tend to vary independently of the conditions to which they in their progenitors had been exposed. Whilst others maintain that all variation is due to such exposure. Though the manner in which the environment acts is yet quite unknown. At the present time, there's hardly any question biology of more importance than this of the nature and cause of variability. So I think evenness today, I think that even today there's hardly any question of biology a more important than how variation and how inheritance work. And so it is close by, by just suggesting three books if you want to read more. Read more about the discovery of the gene and some current research on it. This is fantastic book by Siddhartha Mukherjee is highly recommended. If you want know more about non-genetic inheritance, like epigenetic inheritance. This book in the middle by Russell bond Raskin Troy day on extended heredity is very, a very easy read and great but yet very scholarly. And then lastly, if you want know more about plasticity of evolution, you might want to consider this book on the far right. But importantly, this book which I had just came out this past summer, this book is available for free download it Taylor and Francis at the publishers websites, you're going to go out and spend a lot of money on the book. You can just download it and read it on your, on your reader. And so with that, thank you very much again for the invitation and for hosting this symposium and thanks a lot. Thank you. Um, I think we can take a few questions. If anybody has some. Just speak up. If you have a question. David, I, I'd like to ask whether you think this was a major paradigm shift. So yeah, I don't like to get into the kinds of debates. I think that it could be interpreted that way. And some people have suggested that there there had been, you know, there was there was a point, counterpoint back in 2014. And nature by two groups of very distinguished scientists are arguing that incorporating plasticity epigenetics into evolutionary theory was kinda, cars are revamping of evolutionary theory. And another group said, no. I think that it's important to realize that first of all, these ideas have been around for a long time, right? So many of these ideas are not new ideas. And as I tried to indicate the beginning, they go way back. And indeed one of things I didn't emphasize enough at the beginning is that Lamarck is often credited with the inheritance of acquired characters. But that wasn't he really has key idea. This idea had been around for at least two millennia. And so I think that, you know what, your Darwin didn't know about genes, right? All Darwin knew is that like beget, like, and so if that's mediated by a DNA base pair sequence changes, works. If it's mediated by nearby methyl marks, it works potentially too. And so it doesn't undercut sort of understanding of how natural selection works. And so I, I don't think it's so much a paradigm shift is maybe just, you know, thinking about things a little more broadly. One of the things that also strikes me too, by the way, is that I'm at a university that's, you know, we don't, we haven't evolution group here, but we're not like, we're not like one of the strongest evolution groups in the world. We do have an incredible medical school here. And so I go to talks over the medical school all the time. And the medical researchers have been on this for a long time, right? They understand epigenetics, they understand its importance and they're not arguing about it. They're just going where the data are, taking them and says, I think it's evolutionary biologists to connect the last group of people that are sort of being brought along into this thinking about the role of the environment plays in both generating traits but also in influencing how inheritance works. Aaron and I belong to an evolutionary medicine group which has had very interesting discussions on this regard. Yes. Well, if we don't have questions, way it I'm very impressed that we still have had almost 50 people staying with us for this long evening. We invite you to tomorrow evening where we have four more speakers were deleted every year to celebrate this group of incredible people who have crossed so many different disciplines. And we have had, you know, from agriculture and medicine and evolutionary biology and history. And tomorrow night we have two philosophers as well, as well as another kind of shed at educational kinds of issues as well. And so we invite you to read, join us tomorrow evening. And we thank you so much for coming. And if you can turn your cameras on for a second, just that give an applause to our speakers. Made it really is so wonderfully important. So thank you. Karen, a closing remark. I don't have the zoom thing yet, but see you too. Thanks everyone. We're greatly appreciative. Thank you, David very much. Thanks. We will ever go. Thank you. Thanks, Dr. Scott. We look forward to seeing you tomorrow. Thanks, Mark. Okay. I see it.
International Darwin Day 2/15
From Courtney O'Brian March 07, 2022
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Charles Darwin was born on 12 February 1809. The University of Delaware will join event organizers from around the world to virtually celebrate Darwin’s contributions to humanity, science and rational thought with talks by scientists and scholars on a variety of related topics over two nights.
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- Biological Sciences, Anthropology
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- February 15, 2022
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