Dr. Sarah Tishkoff | Tishkoff Lab

Sarah Tishkoff is the David and Lyn Silfen University Professor in Genetics and Biology at the University of Pennsylvania, holding appointments in the School of Medicine and the School of Arts and Sciences. She is also Director of the Penn Center for Global Genomics and Health Equity.

Dr. Tishkoff studies genomic and phenotypic variation in ethnically diverse Africans. Her research combines field work, laboratory research, and computational methods to examine African population history and how genetic variation can affect a wide range of traits – for example, why humans have different susceptibility to disease, how they metabolize drugs, and how they adapt through evolution.

Dr. Tishkoff is a member of the National Academy of Sciences and a recipient of an NIH Pioneer Award, a David and Lucile Packard Career Award, a Burroughs/Wellcome Fund Career Award, an ASHG Curt Stern award, and a Penn Integrates Knowledge (PIK) endowed chair. She is a member of the Scientific Advisory Panel for the Packard Fellowships for Science and Engineering and the Board of Global Health at the National Academy of Sciences and is on the editorial boards at PLOS Genetics, Genome Research; G3 (Genes, Genomes, and Genetics);Cell.

Her research is supported by grants from the National Institutes of Health, the National Science Foundation, the Chan Zuckerberg Institute, and the American Diabetes Association.

Abstract:

Africa is the ancestral homeland of all modern human populations within the past 300,000 years.  It is also a region of tremendous cultural, linguistic, climatic, phenotypic and genetic diversity.   Despite the important role that African populations have played in human history, they remain one of the most underrepresented groups in human genomics studies. A comprehensive knowledge of patterns of variation in African genomes is critical for a deeper understanding of human evolutionary history and the identification of functionally important genetic variation that plays a role in both normal variation and disease risk.  Here I will describe our studies of genomic variation in ethnically and geographically diverse Africans in order to reconstruct human evolutionary history and identify candidate genes that play a role in adaptation to infectious disease, diet, high altitude, stature, and skin color. I will highlight recent research integrating data from a genome wide association study of skin pigmentation in Africans and scans of natural selection from whole genome sequencing. Combining high-throughput reporter assays, Hi-C, CRISPR-based editing, and melanin content assays, we identified novel regulatory variants that impact melanin levels in vitro and modulate human skin color variation. Additionally, we identified a novel gene regulating pigmentation by impacting genes involved in oxidative phosphorylation and melanogenesis. These results provide insights into the mechanisms underlying human skin color diversity and adaptive evolution.

Watch the seminar here!

Dr. Bryan Dewsbury | Dewsbury Lab

Bio:

Bryan Dewsbury is an Associate Professor of Biology at Florida International University where he also is an Associate Director of the STEM Transformation Institute. He received is Bachelors degree in Biology from Morehouse College in Atlanta, GA, and his Masters and PhD in Biology from Florida International University in Miami, FL. He is the Principal Investigator of the Science Education And Society (SEAS) program, where his team conducts research on the social context of education. He is a Fellow of the John N. Gardner Institute and a Director at RIOS (Racially-Just Inclusive Open Science) institute. He conducts faculty development and support for institutions interested in transforming their educational practices pertaining to creating inclusive environments and, in this regard, has worked with over 100 institutions across North America, United Kingdom and West Africa. He is a co-author of the book 'Norton's Guide to Equity-Minded Teaching', available for free as an E-book. He is the founder of the National Science Foundation (NSF) funded Deep Teaching Residency, a national workshop aimed at supporting faculty in transforming their classroom to more meaningfully incorporate inclusive practices. He is the creator of the MOOC called 'Inclusive Teaching' sponsored by HHMI Biointeractive which will be released on August 15th. Bryan is originally from the Republic of Trinidad and Tobago and proudly still calls the twin island republic home.

Abstract:

Education holds the promise of preparing students to be engaged, thriving participants in a socially just democracy. For that ideal to occur, the structure and experience of the classroom must reflect both its constituents and consider the socially just imaginaries in which we would all like to inhabit. Using examples from the civil rights era's interrogation of our society, we will explore how an introductory biology course can help fulfill higher

education's civic mission.



Check out his book here!

Check out his HHMI/Inclusive Teaching trailer here!



Watch the seminar here!

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.

Check out the seminar here!

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. Joseph L Graves, Jr.

Bio:

Dr. Joseph Graves, Jr. received his Ph.D. in Environmental, Evolutionary and Systematic Biology from Wayne State University in 1988. In 1994 he was elected a Fellow of the Council of the American Association for the Advancement of Science (AAAS.) In 2012, he was chosen as one of the “Sensational Sixty” commemorating 60 years of the NSF Graduate Research Fellowship Award.  In 2017, he was listed as an “Outstanding Graduates” in Biology at Oberlin College; and was an “Innovator of the Year” in US Black Engineer Magazine.

His research in the evolutionary genomics of adaptation shapes our understanding of biological aging and bacterial responses to nanomaterials. He is presently Associate Director/co-PI of the Precision Microbiome Engineering (PreMiEr) Engineering Research Center of Excellence (Gen-4 ERC) funded by the National Science Foundation (2022—2027). He has published five books: A Voice in the Wilderness: A Pioneering Biologist Explains How Evolution Can Help Us Solve Our Biggest Problems, (New York: Basic Books), 2022; with Alan Goodman, Racism, Not Race: Answers to Frequently Asked Questions, Columbia University Press, 2022. Racism, Not Race was named by Kirkus Reviews as “One of the Best Non-Fiction 2021” and to its “Best Books About Being Black in America 2021”; Principles and Applications of Antimicrobial Nanomaterials, (Amsterdam NE: Elsevier),  2021; The Emperor's New Clothes: Biological Theories of Race at the Millennium, Rutgers University Press, 2005 and The Race Myth: Why We Pretend Race Exists in America, Dutton Press, 2005.

He leads programs addressing underrepresentation of minorities in science. He has aided underserved youth in Greensboro via the YMCA chess program.  He has also served on the Racial Reconciliation and Justice Commission, and COVID Vaccination Task Fore of the Episcopal Diocese of North Carolina. He also served as the science advisor to the Chicago, New Brunswick, and Methodist of Ohio Theological Seminaries through the AAAS Dialogues of Science, Ethics, and Religion (DoSER) program.

Abstract: 

In A Voice in the Wilderness, I discuss the story of how I became the first African American evolutionary biologist.  It was a life of strife that followed me everywhere I went. I was beset by imposter syndrome, by depression, by racism, by negligence, and contempt.  And yet I persevered and became a prominent scholar in evolutionary biology.  I have helped to lead the fight against scientific racism, utilizing my science a tool to resist exploitation and change the demography of the scientific enterprise.



Check out his most recent article here!

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. Maria Barna | Barna Lab

BIO:

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.

Abstract:

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.

Check out the seminar here!

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.

Watch the seminar here!

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.

Molly Womack 

Womack Lab