Biology Ribble Endowment Seminar
I am an evolutionary ecologist interested in how climate and landscape history shape the
diversity, biogeography, and ecological structure of mammalian faunas across spatio-temporal
scales. I test hypotheses about how changes in climate, tectonic activity, topographic
complexity, and habitat heterogeneity impact communities and ecological processes at local
scales and govern diversity at regional scales. To do so, I use the fossil record to investigate
diversity patterns, macroevolutionary processes, and paleoecology, focusing on the history of
small mammals during the Cenozoic. My work on the past is conducted in parallel with
investigations of modern and historical small-mammal populations across broad climatic and
environmental gradients today.
My research group integrates fieldwork, specimen-based research, and quantitative
paleobiology. Primary tools of our research include stable isotope ecology and
paleoenvironmental reconstruction, analysis of trait variation, diversification analysis, and
coupling of geological and biological modeling approaches. We work in western North
America and in the East African Rift, both tectonically active and dynamic landscapes with
high species richness today and in the past.
Mountains across the globe are biodiversity hotspots for many different groups of plants and animals; however, the deep-time relationship between mountain building and biodiversity remains elusive and requires integration across disciplines in geosciences, paleontology, and biology. When and how did these hotspots form? What role do landscape and climate dynamics play in eco-evolutionary processes? Using modern and fossil records, as well as empirical and quantitative approaches, my research program investigates how the biodiversity of mammals has been influenced by tectonic and climate interactions that shape mountain landscapes and generate topographic and climatic gradients. In this presentation, I will focus on the diversification history and faunal structure of mammals in the Basin and Range Province of western North America across the Neogene, highlighting the role of tectonic extension and global warming during the Miocene Climate Optimum (17-14 million years ago) at multiple spatial scales. I will also share new research from coupled landscape-biotic evolution models to understand how tectonic uplift may both generate and preserve evidence of montane biodiversity hotspots in the fossil record.
Watch the seminar here!
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.
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"Calculating Collapse and Stability of Food Webs Based on Consumption Constraints, Body Size, and Changing Temperature"
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.
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
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.
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.
"Ribosomes in Gene Regulation: Controlling the Diversity of Proteins Made in Specific Cells, Tissues, and Organisms"
Dr. Barna obtained her B.A. in Anthropology from New York University and her Ph.D. from Cornell University, Weill Graduate School of Medicine. Dr. Barna was subsequently appointed as a UCSF Fellow through the Sandler Fellows program, which enables exceptionally promising young scientists to establish independent research programs immediately following graduate school. She is presently an Associate Professor in the Genetics Department at Stanford University. Dr. Barna has received a number of distinctions including being named a Pew Scholar, Alfred P. Sloan Research Fellow, and top ’40 under 40’ by the Cell Journal. She has received the Basil O’ Connor Scholar Research Award and the NIH Directors New Innovator Award. She is the recipient of the Elizabeth Hay Award, H.W. Mossman Award, Tsuneko and Reiji 'Okazaki Award', American Society for Cell Biology Emerging Leader Prize, the Rosalind Franklin Young Investigator Award, and the RNA Society Early Career Award. She is presently a NYSCF Robertson Stem Cell Investigator.
Work from our lab has changed the view that ribosomes are passive, indiscriminate machines. Our studies suggest that the translation machinery is a more dynamic, macromolecular complex with complex and specialized roles in the cell. A major interest in the lab is centered on understanding how ribosomes dictate when and where proteins are made to direct rapid and dynamic cell fate transitions. We study both the functional roles of ribosomes in normal mammalian development and in disease states such as ribosomopathies. We employ a wide-variety of technologies including mass spectrometry, sub cellular resolution imaging, as well as sequencing platforms to characterize ribosomes and their variation at the level of protein, rRNA, and modifications. Ultimately, the goals of the lab are to know how ribosomes function in sub cellular space, across different cell types, and the biological meaning of ribosome-mediated control of gene expression towards organismal development and evolution. Our recent research efforts are also centered on understanding how changes in the translatome influence tissue regeneration and regenerative potential across different kingdoms of life.
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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).
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.
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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.
Insect species distributions are tightly linked to winter conditions. Surviving winter requires adaptations to cope with low temperatures and limited food resources, and much of our lab’s work focuses on the underlying mechanisms used by insects to survive extreme winter conditions. In this talk, I will primarily discuss our recent work on survival mechanisms of the Antarctic midge, which is the world’s southernmost insect and the only species endemic to Antarctica. This species can survive freezing of its body fluids for up to nine months a year, but it must also cope with considerable spatial and temporal variability in Antarctica’s unpredictable environments. Here, I will summarize how this impressive beast survives internal freezing, as well as the consequences of microhabitat variability and winter climate warming.
Larvae (left) and adults (right) of the Antarctic midge
Abstract: A graduate student’s relationship with their research advisor is considered to be the single-most influential factor in the quality and outcomes of their graduate training experience. Indeed, effective mentorship by research advisors promotes the development and success of graduate mentees. Yet, mentoring relationships, like any prolonged relationship, can have negative elements. Little research has examined the problematic elements of graduate research mentoring, even though prior research on mentoring in workplace settings suggests that negative mentoring experiences are common. This seminar will present findings from research on the negative mentoring that graduate life science researchers experience, including how their experiences differ from negative mentoring experienced in workplace settings. The session will offer insights on how mentor behaviors may be experienced as harmful or unhelpful and on how mentees and mentors can identify, avoid, and mitigate the impacts of negative mentoring.