Dr. Francois Spitz | Spitz Lab

Bio:
PhD from Université Paris 6 (France)
Group Leader at the European Molecular Biology Laboratory (2006-2015) (Heidelberg, Germany)
Head of Research Unit at the Institut Pasteur (2015-2019) (Paris, France)
Professor, The University of Chicago (2019-.)

Abstract:
The mechanisms that regulate the efficiency and specificity of interactions between distant genes and cis-regulatory elements such as enhancers play a central role in shaping the specific regulatory programs that control cell fate and identity. In particular, the (epi)genetic elements that organize the 3D folding of the genome in specific loops and domains have emerged as key determinants of this process. I will discuss our current views on how 3D genome architecture is organized, how it influences gene regulatory interactions and illustrate how alterations of the mechanisms and elements that organize genomes in 3D could contribute to genomic disorders and genome evolution.

Dr. Blake Meyers | Meyers Lab

BIO: 
Blake Meyers is a Member & Principal Investigator at the Donald Danforth Plant Science Center in St.
Louis, and he is a Professor in the Division of Plant Science and Technology at the University of
Missouri - Columbia. He formerly held the Edward F. and Elizabeth Goodman Rosenberg
professorship at the University of Delaware, where his research group was from 2002 to 2015. He
was elected as a Fellow of the American Association for the Advancement of Science (AAAS) in 2012,
and a Fellow of the American Society of Plant Biologists (ASPB) in 2017, the same year he was
awarded the Charles Albert Shull Award by the ASPB for outstanding investigations in the field of
plant biology. He was elected to the US National Academy of Sciences in 2022. After serving on the
editorial board since 2008, Blake became the Editor-in-Chief of The Plant Cell in January 2020. Work
in his lab addresses the biological functions, biogenesis, genomic impact, and evolution of small
RNAs in diverse plant species, using combination of genomic and molecular genetics approaches,
with a focus on phased, secondary siRNAs (“phasiRNAs”).

He received his undergraduate degree in biology from the University of Chicago in 1992, and
working with Prof. Richard Michelmore at UC Davis, was awarded M.S. and Ph.D. degrees in genetics in 1995 and 1998, respectively. After that, he did a postdoc with Prof. Michele Morgante at DuPont Crop Genetics, working on maize genomics for 2 years before returning to Prof. Michelmore’s group at UC Davis in 2000 to do a 2nd postdoc on Arabidopsis disease resistance. In 2002, Blake started his
own research group at the University of Delaware. He was the chair of the Department of Plant & Soil Sciences at the University of Delaware from 2009 to 2015.

Abstract:
In plants, 21 or 22-nt miRNAs or siRNAs typically negatively regulate target genes through mRNA cleavage or translational inhibition. Heterochromatic or Pol IV are 24-nt and function to maintain heterochromatin and silence transposons. Phased “secondary” siRNAs (phasiRNAs) are generated from mRNAs targeted by a typically 22-nt “trigger” miRNA, and are produced as either 21- or 24-mers via distinct pathways. Our prior work in maize and rice demonstrated the temporal and spatial distribution of two sets of “reproductive phasiRNAs”, which are extraordinarily enriched in the male germline of the grasses. These two sets are the 21-nt (pre-meiotic) and 24-nt (meiotic) siRNAs. Both classes are produced from long, non-coding RNAs, generated by hundreds to thousands of loci, depending on the species. These phased siRNAs show striking similarity to mammalian piRNAs in terms of their abundance, distribution, distinctive staging, and timing of accumulation, but they have independent evolutionary origins. The functions for these small RNAs in plants remain poorly characterized. I will describe our recent work investigating the functions of plant phasiRNAs and their roles in modulating traits of agronomic importance in plants, including male fertility, as well as novel applications of phasiRNAs such as those generated from transplastomic plants.

Ned Dochtermann | Dochtermann Lab

Abstract:
While behavioral syndromes are frequently argued to represent an optimal outcome of correlated selection, they also have the potential to constrain evolutionary responses. Via intraspecific and interspecific comparisons we attempted to determine whether behavioral variation was distributed in a manner consistent with either (or both) of these explanations. We compared the distribution of genetic variation across four populations of field crickets (Gryllus integer) and for seven behavioral measures. The distribution and orientation of genetic variation was conserved across populations and divergence among populations was constrained to a shared direction in multivariate space. We then compared the distribution of behavioral variation across five species of crickets and identified a strong phylogenetic signal. Combined, these intra- and interspecific comparisons are consistent with behavioral syndromes acting as constraints on evolutionary outcomes. Finally, in a natural population of deer mice (Peromyscus maniculatus) we compared the orientation of behavioral variation with the direction of selection acting on the population. We found that the distribution of behavioral variation was inconsistent with our a priori predictions. These three independent results suggest that intuitive adaptive explanations may be insufficient to explain the ubiquity of behavioral syndromes.

Dr. Van Savage

Bio:
I am a Professor in the Ecology and Evolutionary Biology and Biomathematics departments. A major goal of my research is to quantify and understand the possible functions, forms, and interactions of biological systems that result in the extraordinary diversity in nature. I have studied a wide range of areas such as metabolic scaling, consumer-resource interactions, rates of evolution, effects of global warming on ecosystems, tumor growth, and sleep. Complementary to this, I aim to understand how much variation around optima or averages is considered healthy or adaptive versus diseased or disturbed states, which are essentially deviations from normal or sustainable functioning. As I attempt to make progress on these questions, I join together ecology, evolutionary theory, physiology, mathematical modeling, image-analysis software, informatics, and biomedical sciences. Many theories, including some of my work, focus on optimal or average properties, but more recently, I have been working to obtain the large amounts of data necessary to characterize variation in key properties. My new findings about the diversity and variation in form and function are revealing flaws in current models, and I am working to develop new theories that incorporate realistic amounts of natural variation.

Abstract:
The question of which factors contribute to ecosystem and food webs stability is one of the most fundamental and foundational in all of ecology. Here I present findings from a new numerical model that allows us to include or exclude different potential factors, and I interpret these results using a novel method that examines how stability and connectance change with consumer-resource size ratios. In this way we are able to compare our predictions and model with empirically grounded data and known trends. Consequently, we are also able to study how variation in size distributions within food webs overall impact the stability of food webs. These results are followed by a more analytical mathematical treatment of how eigenvalue distributions—directly related to system stability—change depending on the structure of the interaction matrix. As part of this, I review and revisit seminal work by Robert May and Stefano Allesina, and connect with and synthesize some lesser known theorems from linear algebra to illuminate and understand some of the results from our numerical model. Finally, I talk about how this work might be extended to consider the impacts of increasing or fluctuating temperatures due to climate change, and possible directions for enlarging and extending the
mathematical concept of stability to something closer to its ecological meaning.

Dr. Rafael Demarco | Demarco Lab

Bio:
I am a new Assistant Professor in the Department of Biology at the University of Louisville whose ultimate goal is to understand how changes in metabolism impact stem cell behavior during homeostasis, aging and stress conditions. I was trained as a geneticist during my Ph.D. with Dr. Erik Lundquist at the University of Kansas, where I learned to ask questions and interpret genetic data using model organisms. To pursue my objective of studying stem cells and their niches, I obtained my postdoctoral training and later position as a Research Specialist in the laboratory of Dr. Leanne Jones (first at the Salk Institute and then at the University of California, Los Angeles and San Francisco), a leading expert in the fields of stem cells and current director of the Bakar Aging Research Institute at UCSF. During my time working with Dr. Jones, I developed my own research interests focusing on how different aspects of metabolism impact the stem cell niche present in the Drosophila testis. Unexpectedly, I found that both stem cell populations present in the testis niche employ mechanisms to maintain proper lipid homeostasis in order to prevent stem cell loss. Disruptions in either mitochondrial fusion (in germline stem cells1) or autophagy (in cyst stem cells2) led to deficient lipid catabolism and ectopic accumulation of lipids in the stem cell niche, which promoted stem cell loss through differentiation. Hence, a model has emerged revealing a novel metabolic facet in the regulation of stem cell fate, which appears conserved across stem cell systems3. In my recently established laboratory, I am engaged in pursuing the mechanism(s) through which ectopic lipid accumulation can impact stem cell fate within the niche, which could shed light into the development of new strategies targeting stem cell-based regenerative therapies.

Abstract:
The capacity of stem cells to self-renew or differentiate has been attributed to distinct metabolic states. A genetic screen targeting regulators of mitochondrial dynamics revealed that mitochondrial fusion is required for male germline stem cell (GSC) maintenance in Drosophila melanogaster.  Depletion of Mitofusin (dMfn) or Optic atrophy 1 (Opa1) led to dysfunctional mitochondria, activation of Target of Rapamycin (TOR), and a dramatic accumulation of lipid droplets (LDs). Pharmacologic or genetic enhancement of lipid utilization by the mitochondria decreased LD accumulation, attenuated TOR activation and rescued GSC loss caused by inhibition of mitochondrial fusion. However, the mechanism(s) leading to GSC loss were unclear. TOR activation has been demonstrated to suppress JAK-STAT signaling by stabilizing the JAK-STAT inhibitor SOCS36E. As JAK-STAT signaling is critical for regulating stem cell self-renewal in the testis, we wanted to test the hypothesis that the increase in TOR activity in early germ cells would lead to SOCS36E stabilization, which in turn, could contribute to stem cell loss.  Indeed, we found that SOCS36E levels were higher in early germ cells upon depletion of dMfn or Opa1. Subsequently, we show that activation of the JAK-STAT pathway, but not BMP signaling, is sufficient to rescue loss of GSCs as a result of the block in mitochondrial fusion.  In addition, preliminary genetic and proximity-labeling data suggest that LD accumulation acts in parallel to TOR/SOCS36E to promote GSC loss. Our findings highlight a critical role for mitochondrial metabolism and lipid homeostasis in GSC maintenance, providing a framework for investigating the impact of metabolic diseases on stem cell function and tissue homeostasis.

Dr. Jessica Blois | Blois Lab

BIO:
Dr. Jessica Blois is an Associate Professor in the Department of Life and Environmental Sciences at UC Merced. Her research is particularly focused on examining the relative roles of environmental versus biotic drivers of biodiversity change, in merging data from different kinds of fossil proxies such as mammal bones and plant macrofossils, and in applying perspectives from the past to help conserve biodiversity. Her work combines field work aimed at broadening our samples of fossil and modern mammals, phylogeographic analyses to understand how genetic diversity is structured spatiotemporally, and paleobiogeographic modeling. Dr. Blois’ primary study system is North American mammals from the past 21,000 years, and she also has a strong focus on developing the paleo-informatic infrastructure to enable large-scale science.

Abstract:
Climates today are changing substantially and will continue to do so over the next hundred years and beyond. All of the different elements that comprise Earth’s biosphere—its biodiversity—depend on and respond to Earth’s climate in a variety of ways, and in turn, Earth’s biodiversity modulates the magnitude and trajectory of climate change. Species responses to highly novel climatic (and other anthropogenically-forced) conditions—which may fall outside the range of conditions experienced by species over their histories—will impact the adaptive capacity and evolutionary potential of species and shape future patterns of biodiversity. In this talk, I will present several recent projects illustrating how climate impacts biodiversity. I will focus on ecological processes that structure local populations and communities, and then move towards how we can scale up towards a broader understanding of how ecological processes structure biodiversity patterns across space and time.

Dr. Colin Saldanha

BIO:
Colin J Saldanha received his doctorate in Psychology from Columbia University, conducted postdoctoral research in Neuroendocrinology at UCLA and established his independent research program in the Dept. of Biological Sciences at Lehigh University in 2001. Here he was tenured and later promoted to full professor in 2011. He conducts research on how secreted signals such as steroids are delivered with spatial and temporal precision to targeted locations in the brain to modulate and orchestrate neurophysiology and complex behaviors. He is particularly curious about the pluripotent actions of estrogens on reproductive, aggressive, affiliative, and rewarding behaviors, as well as the modulation of spatial memory, sociality, and neuroprotection. His work has been supported by the National Institutes and Health and the National Science Foundation (NSF). He has published extensively including journals like Endocrine Reviews and Current Biology. He was awarded the Libsch Early Career Award (2003) and the Stabler Award for Excellence in Teaching (2006). Since 2011 he has re-established his research program at the Department of Neuroscience and the interdisciplinary Center for Behavioral Neuroscience at American University (AU). In this capacity he, along with others, have aided the considerable expansion of the natural sciences at this institution. Colin has served as Chair of the Biology Department at AU and as Chair of the Education Committee and Secretary for the Society for Behavioral Neuroendocrinology and is a Member of the BOD of the Federation of Associations in Behavioral and Brain Sciences. He has recently completed a rotation as Program Director and Expert in the Neural Systems Cluster of the Division of Integrative and Organismal Biology at the National Science Foundation.

Abstract:
Hormones like steroids modulate numerous behavioral endpoints, affect several peripheral and central targets, and are often synthesized in multiple tissues. The mechanisms whereby this modulation is achieved with temporal and spatial specificity remain unclear. 17-estradiol (E2) is made in ovaries, placenta, bone, adipose, and in the brain. Neuroestradiol is a potent mediator of a range of behaviors during development and adulthood. How is estradiol delivered to the right target, at the right time, and at the right concentration? Perhaps more importantly, how is it that multiple E2-dependent targets and behaviors aren’t modulated simultaneously? We have learned that aromatase (estrogen-synthase) can be induced in astrocytes following damage to the brain and is expressed at central synapses. Both mechanisms of estrogen provision confer spatial and temporal specificity on a lipophilic neurohormone with potential access to all cells and tissues. This talk will trace the progress in our understanding of astrocytic and synaptic aromatization in both in reactive astrocytes and at central synapses. The talk will end with relatively novel hypothesis regarding the role of neuroestradiol in the orchestration of species-specific behaviors.

Dr. Tesla Monson | Monson Lab

BIO:
Dr. Tesla Monson is an Assistant Professor of Anthropology at Western Washington University where she runs the Primate Evolution Lab. Her lab’s research focuses on the evolution of skeletal variation, life history, and reproduction in extant and fossil mammals. Dr. Monson recently published the first methods for reconstructing prenatal growth rates in the fossil record, one of which relies exclusively on teeth. Dr. Monson earned her PhD in Integrative Biology at UC Berkeley (2017), which is where she first became interested in science communication and research. Since then, she has developed and hosted a series of sci-comm projects, ranging from a science talk radio program called The Graduates, to a Twitter series highlighting the influence of women in early Washington State history (Washington Women).

Abstract:
The vertebrate fossil record is comprised almost entirely of the remains of bones and teeth. It is thus a key goal for evolutionary biologists to extract as much information as possible from these anatomical remains through morphological investigation. My research has demonstrated that there are significant phenotypic correlations between many anatomical traits, as well as between craniodental morphology and life history. These correlations both constrain and enable evolution, leading to the morphological diversity and disparity that we see today. In this talk, I will discuss our new research using cranial and dental morphology to reconstruct prenatal growth rates in

the hominid fossil record. Prenatal growth, or how quickly a fetus grows in utero, varies widely across primate species with the highest rate in humans. We recently demonstrated that prenatal growth rates increased throughout the Pleistocene, reaching ‘human-like’ rates just under 1 million years ago, before the evolution of our species. Prenatal growth is also key to healthy pregnancy and delivery. I will end by presenting some of our ongoing and future research investigating prenatal growth, and the evolution of encephalization and body size in primates.

"Fossil teeth reveal how brains developed in utero over millions of years of human evolution-new research"

Watch the seminar here!

Hugo Reyes-Centeno HEVA (Human Evolution & Virtual Anthropology Lab) EduceLab

Dr. Hugo Reyes-Centeno is an evolutionary anthropologist specializing on the emergence of modern human anatomy and behavior over the last million years. In addition, he conducts inter-disciplinary research on human biocultural diversity and the study of natural and cultural heritage worldwide. Prior to joining the University of Kentucky in 2020 as Assistant Professor of Anthropology, he served as Scientific Coordinator and co-founder of the Center for Advanced Studies “Words, Bones, Genes, Tools” at the University of Tübingen (Germany), where he also completed a dissertation in the Institute of Archaeological Science and the Senckenberg Centre for Human Evolution and Paleoenvironments. His research has appeared in Cell, PNAS, Journal of Human Evolution, and PLoS Genetics, among other venues. He has performed paleontological and archaeological fieldwork in France, Italy, Peru, the Philippines, and Spain. Currently, he serves as Co-PI of the NSF-funded EduceLab: Infrastructure for Next Generation Heritage Science.

Abstract: Despite consensus on the emergence of anatomically modern humans in Africa and their subsequent dispersal into the rest of the world, the mode and timing of these processes remain controversial topics. In addressing them, data on human anatomical and genomic variation have sometimes generated conflicting inferences. Therefore, approaches that consider both lines of evidence under a common theoretical framework are important for reconciling competing evolutionary models. In this talk, I highlight research that tests competing models of human dispersal out of Africa, which applies quantitative genetic and population genetic methods to anatomical and genomic data. I discuss the caveats of these conclusions, including the influence of admixture between modern humans and other hominins. Furthermore, I examine how these findings align with the known human fossil record and a growing inventory of ancient genomes from archaeological and paleontological contexts. Finally, I review how ongoing field and laboratory projects in Eastern Africa, Southeast Asia, and South America shed light on human evolution, adaptations, and dispersals.

Christopher Schell ESPM Christopher Schell UC Berkeley

Bio:

Dr. Chris Schell is an Assistant Professor in the department of Environmental Science, Policy, and Management at the University of California Berkeley. Dr. Schell’s research focuses on the behavior, physiology, and health of wildlife in cities. Specifically, he and his lab investigate how urban infrastructure, environmental stressors, and human-wildlife interactions shape the phenotypic traits of mammalian carnivores, mainly coyotes and raccoons. Because the distribution of such attributes is often governed by societal inequities (e.g., socioeconomic, racial, etc.), Schell and his team also spotlight the need to incorporate an environmental justice and One Health lens into urban ecological research. Further, he is committed to community engagement and science communication, collaborating with organizations like the Cal Academy of Sciences, Oakland Zoo, East Bay Regional Parks, Doris Duke Scholars Conservation Program, and California’s 30x30 initiatives.

Abstract:

Past ecological processes and phenomena often have broad implications for contemporary habitat conditions and ecosystem structure. Long-term ecological research, for instance, has provided extraordinary insight into the processes that influence primary and secondary succession, population growth rates, community assemblages, and nutrient cycling. Similarly, past societal legacies have profound impacts on current societal processes, with much of our current reality shaped by policies enacted decades past. These social and ecological legacies are often most apparent in cities, where humans and their constructed ecosystems coalesce. It is in these environments that we have a unique opportunity to interrogate how our past shapes our social-ecological present. Necessarily, understanding how past societal processes have contributed to shaping current ecosystem processes is key to building predictive models and resilient systems for our future. In this talk, Dr. Chris Schell will explore how one of those legacies in particular – residential segregation via redlining – stratified people and resources, influencing myriad biophysical properties of the city that we currently experience. In doing so, he will discuss how urban evolutionary ecology research can serve to amplify how inequities in society drive ecological disparities in and outside of urban landscapes.

Click here to watch the seminar!