A new associate editor is joining GENETICS in statistical genetics and genomics. We’re excited to welcome Lei Sun to the editorial team.

Lei Sun
Associate Editor
Lei Sun is a Professor in Statistics and Biostatistics at the University of Toronto. She studied mathematics at Fudan University and obtained her PhD in statistics from the University of Chicago in 2001. Her research area is in statistical genetics and genomics, with a focus on robust association methods, multiple hypothesis testing, selective inference, and more recently methods for the X chromosome. In 2017, she received the prestigious Centre de recherches mathématiques-Statistical Society of Canada Prize in Statistics, and in 2020, she served as the President of the Biostatistics Section of the Statistical Society of Canada.

An international collaboration reveals the genetic secrets of endangered species.

Butternuts are soft and oily, with a light walnut flavor that lingers on the tongue. But few Americans have tasted this endangered native. Now, University of Connecticut undergraduates have published the first full map of the unusual tree’s DNA in G3: Genes|Genomes|Genetics.

The butternut is just the first in an ambitious effort to record the DNA of overlooked endangered species before they’re gone. Pumpkin ash, deep sea zigzag coral, and the red-vented cockatoo are a few of the other organisms whose genes are getting thoroughly sequenced by the Biodiversity and Conservation Genomics team at the University of Connecticut’s Institute for Systems Genomics. The program provides undergraduates with a full year of training in how to sequence, reconstruct, and describe the full genetic code of a single species. Other members of the team include Oxford Nanopore Technologies and scientists at the Institute for Systems Genomics (ISG). Students working on specific species also collaborate with people on the ground making restoration and conservation decisions. For the butternut, this includes the US Department of Agriculture Forest Service.

What all the organisms they’re sequencing have in common is that they are endangered species that don’t have a history of major agricultural, medical, or scientific uses.

The butternut Juglans cinerea, for example, is a species of walnut native to North America that looks similar to black walnut but has elongated nuts that are very oily. It was occasionally collected for its oil and harvested for its wood. Butternut trees are now disappearing as a fungus imported from Asia kills them off, with the few survivors tending not to be pure butternut but rather hybrids of Japanese walnut, which interbreeds with butternut easily and has some fungal resistance. Pumpkin ash is one of the 16 species of North American ash being killed off by emerald ash borer insects. The red-vented cockatoo is critically endangered by habitat loss and poaching for pets. And deep-sea corals are threatened by the acidification of the oceans, which threatens their ability to create their skeletons of calcium carbonate.

Many of these organisms are not well studied scientifically. Until recently it was extremely time consuming and costly to sequence an organism’s DNA. Often there are no reference genomes, or full sequences of their genetic code, for entire families of organisms.

“Deep sea coral genomes are incredibly sparse. There are two published out of 5,000 species! This one could be the third,” says ISG Director and genome biologist Rachel O’Neill, who is a co-investigator on the project.

Deep sea coral genomes are particularly interesting because deep water, much like ocean acidification, makes it difficult for corals to grab calcium carbonate out of the water, and yet deep sea corals manage to do it anyway. Understanding which of the genes make this possible could also help us understand how shallow water corals could survive acidification.

Other organisms might have other secrets. Fungal diseases spread by the horticultural trade are rapidly killing off trees in the great forests of Asia, Europe, and the Americas. Sequencing the genomes of related species that evolved with different diseases—such as the butternut and the Japanese walnut—could give valuable insights into which genes provide which type of resistance. It might enable us to save species by replacing a single gene. Even though the Japanese walnut is not endangered, the team is sequencing its genome this year, for this very reason.

“We’re interested in knowing how much of the butternut population is already hybridized with Japanese walnut, and what is contributing to the genetic resistance,” to the fungal infection, says computational biologist Jill Wegrzyn, lead investigator on the team.

And in addition to the practical interest in sequencing these genomes, it’s also interesting simply because they are different from anything else anyone has ever looked at. The ploidy, or number of chromosome copies, can be wildly different than anyone had assumed. Most animals are diploid: they have two copies of each chromosome, one from mom and one from dad. Some plants can be tri- or tetraploid, meaning they have three or four copies of each. But the pumpkin ash tree the team is sequencing this year goes way beyond.

“It’s…maybe…octaploid!” says Emily Strickland, a University of Connecticut student. She started work on the pumpkin ash as an independent research project, found it rather more complex than anyone expected, and is now working on it as part of the Biodiversity and Conservation Genomics team.

The program started last year with a grant from the University of Connecticut, College of Liberal Arts and Sciences Earth and Its Future initiative, and has subsequently been supported by the ISG, with material support from Oxford Nanopore Technologies and Org.one, of which the Center for Genome Innovation in the ISG is an international partner. Org.one is an Oxford Nanopore project to develop high quality assemblies of the genomes of a number of critically endangered plant and animal species. Oxford Nanopore’s DNA/RNA sequencing technology offers real-time analysis that can sequence any length of fragment, from short to ultra-long, and flexibility that is necessary for assembling reference genomes. If the genome was a book, this would be whole phrases instead of single words, making it much faster to assemble.

For many of the 11 undergraduates on the project, this is their first research experience. And several of them chose it because of its practical impact.

“I really liked the idea of using computational techniques to solve problems immediately. On the conservation side, we can do so much,” says Emily Trybulec. She was one of the team members who sequenced the butternut genome last year and wrote the paper they’ve just published, and she’s returned as a mentor this year. Other students point out that doing real research as a part of this project is completely different from a typical classroom experience in which everything is designed to work.

“It forces you to reach out and collaborate, and look for answers yourself, before you ask for help,” Harshita Akella says.

The Biodiversity and Conservation Genomics team’s reference genome of the butternut tree can be found here: https://gitlab.com/PlantGenomicsLab/butternut-genome-assembly.

A new associate editor is joining GENETICS in population and evolutionary genetics. We’re excited to welcome Konrad Lohse to the editorial team.

Konrad Lohse
Associate Editor

Konrad Lohse is a population geneticist interested in learning about evolution in natural populations from genomic data. After a BSc at the University of St Andrews, he obtained a PhD at Edinburgh University under the mentorship of Nick Barton and Graham Stone working on inference of population history. Konrad is currently a Senior Lecturer at Edinburgh University, and he leads a research group that combines theoretical work on the coalescent with genomic studies of adaptation, chromosome evolution and speciation in insects (including various species of butterflies and Drosophila). His group has developed a coalescent-based method to scan genomes of recently diverged taxa for barriers to gene-flow.

A new associate editor is joining GENETICS in the population and evolutionary genetics section. We’re excited to welcome Thomas Lenormand to the editorial team.

Thomas Lenormand

Associate Editor

Thomas Lenormand is Centre National de la Recherche Scientifique research director at the CEFE laboratory. He is an evolutionary geneticist, combining mathematical theory, statistical developments, laboratory experiments, and field work. His work covers a wide range of issues at the intersection of evolution, genetics, and ecology. He is mainly interested in adaptation, the evolution of genetic systems (sex, asex, meiosis, recombination, sex chromosomes) and the effect of mutations. He was an editor and an associate editor of several evolutionary biology journals, twice an European Research Council laureate, and a Harvard Radcliffe fellow. He has received several awards, including the Dobzhansky Prize from the Society for the Study of Evolution.

William Gilliland

Associate Editor

I have been a faculty at DePaul University in Chicago since 2009. I study female meiosis in Drosophila, and I’m most interested in topics like the movement of chromosomes through prometaphase I, the population genetics of meiotic genes, and meiotic drive. My biggest contributions to the field were overturning the prevailing model of female meiosis in flies by showing that chromosome congression actually does happen in flies and the identification of the chromatin tethers that appear to be the mechanism by which cells accurately segregate non-exchange chromosomes away from their homologs in the absence of chiasmata.

Several new editors are joining the GSA Journals. We’re excited to welcome Ricardo Zayas to the GENETICS editorial board under the Molecular Genetics of Development section, and on the G3: Genes|Genomes|Genetics board, we welcome Polly Campbell, Kevin Vogel, Joe Parker, and Ricardo Mallarino.

Ricardo Zayas

Associate Editor

Ricardo Zayas is a Professor of Biology at San Diego State University working on regeneration and stem cell biology. He received a Biology BS degree from Fairfield University and a PhD in Biology from Tufts University in the neurobiology of simple behaviors using larval stages of the tobacco hornworm Manduca sexta. Ricardo then completed postdoctoral training in the laboratory of Dr. Phillip Newmark at the University of Illinois at Urbana-Champaign, where he began to study whole-animal regeneration using the planarian Schmidtea mediterranea. The Zayas lab uses planarian stem cell-based regeneration as a model to investigate molecular mechanisms underlying neurogenesis and epigenetic regulation of stem cell differentiation.

Polly Campbell

Associate Editor

Polly Campbell is an Associate Professor in the Department of Evolution, Ecology, and Organismal Biology at University of California Riverside. Her current research is on genome evolution in mammals, with a focus sex chromosomes and structural mutations and a fascination with conflict. She holds a BS in Biology from University of New Mexico and a PhD from Boston University where she worked on the evolution and ecology of Old World fruit bats in Southeast Asia. In her postdocs she studied the development and evolution of vocal communication in Neotropical mice (University of Florida), and speciation genetics in house mice (University of Arizona).

Kevin Vogel

Associate Editor

Kevin Vogel is an assistant professor in the Entomology Department at the University of Georgia studying vector biology and host-microbe symbiosis. He received his BS from Michigan State University where he studied microbiology and began his work on insects. He earned his PhD from the University of Arizona in Ecology and Evolutionary Biology where he worked under the mentorship of Dr. Nancy Moran studying how variation in symbiont genomes influenced host biology. He then went to the University of Georgia as a postdoctoral associate with Dr. Michael Strand, where he was a Ruth L. Kirschstein NRSA fellow studying mosquito physiology and host-microbe interactions. Kevin started his own lab at the University of Georgia where his group uses diverse approaches to study the interplay between kissing bugs, their gut microbiome, and the parasite Trypanosoma cruzi. His area of expertise includes insect and bacterial genomics. 

Joe Parker

Associate Editor

Joe Parker is an Assistant Professor of Biology and Biological Engineering at California Institute of Technology in Pasadena. Originally from Wales, UK, he obtained a BSc in Zoology from Imperial College London and a PhD from the University of Cambridge/Medical Research Council Laboratory of Molecular Biology. He moved to Columbia University as a postdoctoral fellow, and while in New York also became a Research Associate of the American Museum of Natural History. Joe’s research addresses how relationships between species emerge during evolution. His lab has pioneered a unique model system, the rove beetles (Staphylinidae)—a remarkable clade in which numerous lineages have evolved from free-living predators into behavioral symbionts of social insect colonies. Joe’s work has harnessed this clade to illuminate molecular, cellular, and neurobiological phenomena that shape how animals interact with other living organisms, and evolve to forge new kinds of ecological relationships.

Ricardo Mallarino

Associate Editor

Ricardo Mallarino is an Assistant Professor in the Department of Molecular Biology at Princeton University. His lab is interested in uncovering the molecular mechanisms that give rise to specific morphological, physiological, and behavioral traits, both within a species and over evolutionary time to generate variation across species. To achieve this, his lab develops genomic and experimental resources in emerging mammalian model species that have diverse, ecologically relevant phenotypes and integrates approaches from multiple disciplines, including developmental biology, bioinformatics, and evolutionary genomics. Ricardo received his BSc in Biology from Universidad de los Andes (Bogotá, Colombia) and his PhD from Harvard University. Prior to joining the faculty at Princeton, he was a postdoctoral researcher with Dr. Hopi Hoekstra at Harvard University. Ricardo is a recipient of the Sloan Research Fellowship in Computational and Evolutionary Molecular Biology (2019), the Searle Scholar Award (2019), and the Vallee Scholar Award (2021).

Three new editors are joining GSA journals, GENETICS and G3: Genes|Genomes|Genetics. We’re excited to welcome Arash Bashirullah, Noah Whiteman, and Yun Li to their roles as Senior Advisory Editor for GENETICS, Genome Report Senior Editor for G3, and Associate Editor for GENETICS, respectively.

Arash Bashirullah

Senior Advisory Editor, GENETICS

Dr. Arash Bashirullah is a Professor of Pharmaceutical Sciences in the School of Pharmacy at the University of Wisconsin, Madison where he is also the Associate Dean for Research & Graduate Education. He was an Associate Editor for G3 from 2016-2022; chaired GSA’s International Strategic Planning Group in 2018; and served as an advisor on the GSA’s Early Career Scientist Communication Subcommittee from 2017 to 2019.

Bashirullah’s lab uses genetic, cellular, and molecular approaches to study the hormonal control of animal development with Drosophila as the model organism. The goal of their research is to identify novel genetic and cellular drivers of development and disease.

Bashirullah is responsible for the instruction or coordination of several classes taken by PharmD, BS, and PhD students in the School of Pharmacy. He is also a Faculty Trainer in the Genetics and the Cellular & Molecular Biology Programs at the University of Wisconsin, Madison. As the Associate Dean for Research and Graduate Education, Bashirullah is responsible for the oversight of facilities and processes that support academic research and graduate education in the school. He recently participated in the Academic Leadership Program of the Big Ten Academic Alliance.

Noah Whiteman

Genome Report Editor, G3: Genes|Genomes|Genetics

Noah Whiteman’s research focuses on unraveling the evolutionary histories of interacting species and the genetic basis of adaptations arising from those interactions. They focus on how toxins are a fulcrum around which these species interactions revolve.

Although the systems his lab have studied are diverse, the questions are all about the evolution of species interactions. A strength of their lab is pursuing studies that bridge between model organisms and those organisms that are difficult to study but remarkable in terms of their natural history.

Yun Li

Associate Editor, GENETICS

Yun Li is a statistical geneticist with extensive experiences in method development and application on genotype imputation (developer of MaCH and MaCH-admix), genetic studies of recently admixed population, design and analysis of sequencing-based studies, analyses of multi-omics data including mRNA expression, DNA methylation, chromatin 3D organization, and imaging genetics. She has played an active role in genetic studies of complex human traits resulting in many GWAS and meta-analysis publications, including more than 30 articles in Nature, Science, Cell, and Nature Genetics. Li is leading multiple NIH projects on statistical method development for complex trait genetics. Li has received many awards and was granted the Thomson Reuters Highly Cited Researcher award due to her high impact scientific work. 

Taking direction from evolution

One feature of evolutionary biology that has always intrigued me is the preponderance of “laws.” That is, not “laws” as in Newton’s laws of motion, but less formal ones—analogies and principles that describe a theoretical idea. Many do not have the term “law” attached to them but are laws nonetheless: terms and phrases that describe presumptive fundamental evolutionary phenomena, like the Red Queen hypothesis, Muller’s ratchet, and punctuated equilibrium.

I have a longstanding curiosity about the origins and role of these laws in biology; I think some of them stick around because they help communicate complicated ideas, even if they’re arbitrarily constructed or imprecise.

Dollo’s law is one of my favorite examples:

“An organism is unable to return, even partially, to a previous stage already realized in the ranks of its ancestors.”

In the Blind Watchmaker, Richard Dawkins interpreted it as:

“….just a statement about the statistical improbability of following exactly the same evolutionary trajectory twice (or, indeed, any particular trajectory), in either direction.”

Or even more casually (as I say it):

“It is difficult for an improbable event to happen and then un-happen in the exact same way.”

Essentially, Dollo’s law speaks to the improbability of “reverse evolution.”

Now before you jump in, I know, I know—there are no real directions in evolution. So what am I getting at?

Sure, there is no true “forward” or “backwards” in evolution, and the general misuse of the language of progress has been costly to evolutionary biology. Too many of us (even practicing biologists) tend to erroneously discuss or think about evolution as being a progressive force.

That said, we can discuss direction when we are talking about the evolution of very specific traits in specific settings. For example, if we talk about a population of bacteria evolving resistance to an antibiotic, we can talk about evolving towards resistance (for conversation purposes, at least). “Reverse,” in this situation, would be from a resistant form “back” to a treatable form.

Why is this important?

Well, one of the proposed strategies for preventing the evolution of antibiotic resistance is to drive evolution “backwards.” If a population is resistant to available antibiotics, perhaps we can use drugs to encourage that population to evolve “’backwards” to its more treatable form. Clinicians could then use currently available drugs to treat the newly-non resistant infection.

More recently, scientists have used the term “steering” to talk about ways to manipulate populations of resistant organisms towards being treatable. Physicists and physicians have even used the rules of quantum physics to help think about ways to control the evolution of resistance.

But these applications aside, basic questions surrounding the forces that craft reversal are central in evolutionary theory. The answers are relevant not only for phenomena like antibiotic resistance, but also for other questions about cancer, resistance to butterfly toxins, and more. This even has implications for how we are thinking about genetic modification (GM): when we engineer a mutation into a crop for agricultural purposes, can we be sure that it won’t “un-evolve” that mutation “backwards” towards the non-GM crop?

Asked differently: can evolution do the moonwalk?

What is the moonwalk?

The moonwalk was made famous by Michael Jackson, but it was invented by Shalamar’s Jeffrey Daniel in 1982. We might take it for granted now, but when Daniel first pulled it off, it looked like a special effect. People thought that a string must have been pulling him because he seemed to be moving backwards just as seamlessly and smoothly as one can move forward.

So what does the moonwalk have to do with molecular evolution?

We can ask how evolution might move backwards—just like Daniel’s dance. Equipped with population genetic theory, we can examine the particular forces and conditions that facilitate that backwards movement.

Microbial moonwalking

I have previously published on reverse evolution in the context of antimalarial resistance. In that 2016 study, I found that the surprisingly large impact of certain compensatory mutations limits the ability of a population of resistant malaria parasites to become treatable again. Since then, I have remained curious about other ways to test Dollo’s law: what other places, models, and systems can we use to examine reverse evolution?

Luckily, other scientists I respect and admire had similar curiosities. 

Dr. Pleuni Pennings is an evolutionary computational biologist who helped to pioneer the fusion of classical theoretical population genetics with very modern questions in HIV drug resistance. Her work had a very large impact on my career when I was learning population genetic approaches to thinking about disease evolution during my postdoctoral training. Although we’d already collaborated on several different educational programs and communication efforts, I had never had the pleasure of working with her on an actual science project until she approached me in 2019.

At that time, Dr. Pennings was in the process of establishing a collaboration with Dr. Ruth Hershberg, an eminent microbial evolution expert at Technion-Israel Institute of Technology. Dr. Hershberg had recently published a study that examined the results of experimental evolution in E. coli. Together, they were interested in exploring the conditions that facilitated reverse evolution in experimental populations of E.coli, and they brought me in on the question.

Over the next year or so, we discussed and designed several projects in the arena, but we decided that what we needed first was to use tools in theoretical and computational biology to ask some basic questions:

• How does mutation rate influence the probability of reverse evolution?
• How do the number and phenotypic effect of compensatory mutations influence the probability of reverse evolution?

These are two highly specific but very important variables to investigate for several reasons. For one, Dr. Hershberg had performed experimental evolution in background strains of E.coli that varied in their mutation rate. So we had the potential to compare computational results to experimental findings, which is an important point. Our collaboration provided the opportunity to use models and theory to explain experimental results. Plus, the questions surrounding the effects of mutations were compatible with prior work of mine about the nature and magnitude of compensatory mutations.

To ask these questions about reversion, here’s what we did:

• We created a “computerized world” where a population of bacteria had evolved resistance to a drug. In this situation, resistant variants carried a fitness cost in “drugless” environments, meaning resistant bacteria had high fitness in the presence of drug, but low fitness in the drugless environment.
  
• We then took the drug away (“drugless” environment) and asked whether the population of resistant bacteria would evolve “backwards” towards the wild type ancestor. We might expect this is because wild type had higher fitness than the resistant allele in the “drugless” environment.
  
• We specifically tuned two aspects of evolution in the “drugless” environment: mutation rate and the effect of compensatory mutation, meaning the degree to which mutations compensated for resistance.

The results were fascinating:

• The probability of reverting back to wild type was powerfully influenced by both the mutation rate and the effect of compensatory mutations. At very low mutation rates, compensatory mutations rose to fixation and no reversal to the wild type occurred. At very high mutation rates, compensated reversal emerged. Bacteria evolved two mutations: first the compensatory mutation, then the reversion to the wildtype. Intermediate mutation rates, however, displayed the proper conditions for reversal: the wild type mutation arose early enough that it could dominate a population (Figure 1).
  
• A lot of the findings really did boil down to how strong the compensatory effects were. For mutations that compensate for the cost of resistance: how many are there? Do they fully or partially compensate?

• Critically, the simulation results helped make sense of published experimental results. In these studies, reversal was observed when mutation rates were high. Our modeling result demonstrated that compensatory mutations in the experimental populations likely do not fully alleviate costs associated with resistance.
  
• This is a very big point: our simulations have diagnostic utility. From them, we can walk into experimental data and make sense of them.

In sum, the findings demonstrate how reverse evolution in the context of drug resistance is sensitive to population genetics particulars. 

Why do we care?

For one, simply saying that reverse evolution is unlikely might not be wrong, but it is…incomplete. Population genetics can add color and rigor to this circumstance, so moving forward (no pun intended), all discussions of reverse evolution should be framed in terms of a particular population genetics setting.

Secondly, these results can inform modern conversations around how to steer the evolution of drug resistance. Perhaps we can rationally manipulate populations towards resistance or susceptibility using drugs of various kinds.

So, in the end, we can ask the bigger question:

Can evolution do the moonwalk?

The answer is “Yes, it can”—but the mutation rate and other properties of the context have to be just right.

And this is where the connection between the biology and the dance analogy emerge: you have to be a pretty creative person to come up with something like the moonwalk. But you can’t be too absurd. The innovative step that gave us the moonwalk was the product of an imagination with the right mutation effect size—one that imagines us moving backwards, against our intuition, but still right in rhythm.

Sure people might have been confused by the dance at first, but they will eventually realize that maybe their imaginations were too small and that there is no real forward and backward in dance—just like in molecular evolution.

Congratulations to the winners of the Editors’ Choice Awards for outstanding articles published in GENETICS in 2021! The journal’s Editorial Board considered a diverse range of articles, finding many papers worthy of recognition. After much deliberation, they settled on one exceptional article for each of the three award categories: molecular genetics, population and evolutionary genetics, and quantitative genetics. Check out some of the best GENETICS had to offer in 2021, and be sure to browse the full Spotlight collection.

EDITORS’ CHOICE AWARD IN MOLECULAR GENETICS

Neurogenesis in the adult Drosophila brain

Kassi L Crocker, Khailee Marischuk, Stacey A Rimkus, Hong Zhou, Jerry C P Yin, Grace Boekhoff-Falk

GENETICS Oct 2021, 219(2), iyab092, https://doi.org/10.1093/genetics/iyab092

Crocker et al. describe the Drosophila central brain as a new model in which to investigate adult neurogenesis. The authors observe a significant increase in the number of proliferating cells following injury; they detect new glia, new neurons, and the formation of new axon tracts that target appropriate brain regions. The authors anticipate that this paradigm will facilitate the dissection of the mechanisms of neural regeneration and that these processes will be relevant to human brain repair.

EDITORS’ CHOICE AWARD IN POPULATION AND EVOLUTIONARY GENETICS

The timing of human adaptation from Neanderthal introgression

Sivan Yair, Kristin M Lee, Graham Coop

GENETICS May 2021, 218(1), iyab052, https://doi.org/10.1093/genetics/iyab052

Some Neanderthal-introgressed alleles in modern human populations were adaptive; however, the context in which they provided a fitness advantage is unknown. Yair, Lee, and Coop develop a population genetic method that uses ancient DNA and the hitchhiking effect to determine when natural selection favored the spread of Neanderthal-introgressed alleles. They identify regions of the genome in which Neanderthal alleles were immediately adaptive and others in which there was a significant time lag between admixture and the allele’s rise in frequency.

EDITORS’ CHOICE AWARD IN QUANTITATIVE GENETICS

Why genetic selection to reduce the prevalence of infectious diseases is way more promising than currently believed

Andries D Hulst, Mart C M de Jong, Piter Bijma

GENETICS April 2021, 217(4), iyab024, https://doi.org/10.1093/genetics/iyab024

Quantitative genetic analyses of binary disease status indicate low heritability for most infectious diseases, suggesting that the potential response to selection in disease prevalence is limited. By integration of quantitative genetics with epidemiological models, Hulst, de Jong, and Bijma show that the typical low heritability values of disease status correspond to a substantial genetic variation in disease susceptibility and to a large potential response to selection. Positive feedback mechanisms occurring in disease transmission are crucial for this response and even make eradication of infectious diseases possible. However, current quantitative genetic models ignore these feedback effects and thereby underestimate response to selection in disease prevalence.

Guest post by C Brandon Ogbunu.

2022 marks the return of the Population, Evolutionary, and Quantitative Genetics (PEQG) Conference, organized by the Genetics Society of America. Part of the meeting’s popularity stems from being one of the few conferences that brings together leading thinkers in subfields of genetics that don’t typically overlap, across a range of model organisms, united by methods and perspectives.

The meeting, which will take place June 7-10 in Pacific Grove, CA, at Asilomar Conference Grounds, is well-known for its structure: a combination of keynote addresses, awards, and short talks of various kinds. One of the key aspects of this structure is the session chairs: junior scientists who have established themselves as leaders in the various areas of population, evolutionary, and quantitative genetics. During the meeting, they each chair a session full of talks, and give 30-minute talks of their own during the final keynote session. The session chairs provide an opportunity for us to view the present and future of the field.

The 2022 session chairs promise to deliver on this tradition, featuring a tremendous lineup of thinkers who study problems as diverse as speciation genomics in plants to epistasis in human genomic data sets. This specific collection of speakers displays both breadth and depth, and so the chair keynote session promises to excite.

Below I will highlight these session chairs, commenting briefly on why I am personally so excited to hear about their work.

Nancy Chen

Evolutionary biology is, in part, a science that is defined by information from the past, but how do we use it to ask questions about contemporary evolution in natural populations? These are the questions of the “Pop Gen Chen Lab,” run by Nancy Chen. The lab addresses questions and utilizes tools to think about contemporary questions in short-term evolution, and how genetic variation is maintained in contemporary populations. In addition, the Chen lab makes use of the Florida Scrub Jay (a very compelling and well-studied system) to study population decline. The Chen lab has also generated an extremely useful list of resources on issues related to diversity, equity, and inclusion, and continues to be a leading voice on these matters in the population genetics community. 

Lorin Crawford

Though he was raised in southern California, Lorin Crawford will come to PEQG from balmy New England, where his research program is sprawled out between Microsoft Research in Boston and Brown University (in Providence) where he is the RGSS Assistant Professor. It is difficult to fully capture the richness of his research program. He utilizes advanced statistical and machine learning approaches to directly address provocative questions in population genetics. For example, he has pioneered statistical tests that can be used to detect pairwise epistasis between mutations in large genomic data sets. In addition, his work dissects the architecture of complex traits. Lastly, Crawford has recently begun to explore the ethics of genomics evolution. Recent work in this realm has challenged notions that are used to characterize populations, such as “transethnic.”

Rafael Guerrero

From North Carolina comes Rafael Guerrero, an Assistant Professor at North Carolina State University. He runs a program that develops tools that have already transformed our approach to classical questions in population and evolutionary genetics and explores the questions directly relevant to practical problems in biomedicine and bioengineering. In the former sense, Guerrero has done groundbreaking work on chromosome evolution and hybrid incompatibilities in light of speciation genetics, both central and critical questions in evolutionary genetics. In the latter sense, Guerrero’s mastery of theoretical tools has allowed him to explore areas such as the genomics of adverse pregnancy outcomes, and the physiological determinants of epistatic interactions as they manifest in the evolution of antibiotic resistance.

Priya Moorjani

The Genetics Society of America is well-known for its commitment to model systems research and has long championed its importance. But it also recognizes the importance of human genetics and evolutionary biology, not only because we…are humans, but also because human evolution is an amazing problem space for cutting-edge questions in evolutionary and population genetics. Few scientists are doing more exciting work in this area than Priya Moorjani. Moorjani uses statistical and computational approaches to understand the role of genetic variation in human evolution, demography, and mapping disease risk alleles at the University of California, Berkeley. Moorjani has also investigated fundamental questions in primate evolution, such as the proper estimation of mutation rates. Moorjani has mastered the art of transforming a species that we all care about–Homo sapiens–into a model system in evolutionary genetics. 

Rori Rohlfs

As Assistant Professor at San Francisco State University, Rori Rohlfs won’t need to travel especially far to get to Asilomar, but everything with Rori is an intellectual expedition. Rohlfs runs an exciting program that has examined everything from the evolution of gene regulation to critical statistical questions relevant to genomic testing and forensics. Rohlfs has accomplished this while also being a widely recognized teacher and mentor. Lastly, Rohlfs was one of the corresponding authors on an outstanding 2019 study published in GENETICS that analyzed early population genetics literature and identified the many women that were often denied proper credit for their participation.

Daniel Runcie

When I teach evolution, I often discuss a 2018 study that estimated the biomass of living things on earth, organized by different taxa. Though I do not study plants, I often use it to explain that when it comes to life on earth, plant life is the heavyweight champion. Daniel Runcie runs a thrilling research program that attempts to understand how and why plants are so successful, and especially questions related to genetic variation and phenotypic plasticity. The Runcie lab attempts to identify pathways and networks related to how plants respond to a dynamic environment. One of the reasons that plants have been so successful is their ability to respond to change. The Runcie lab uses a host of tools—statistical, network, and ecophysiological—to understand these questions.

Learn more about the #PEQG22 Session Chairs, as well as Invited Speakers, on the conference website. Registration is open now.

About the author

C. Brandon Ogbunu is Assistant Professor in the Department of Ecology and Evolutionary Biology at Yale University and one of the organizers of the 2022 Population, Evolutionary, and Quantitative Genetics Conference.