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. 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.

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.

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Dr. Michael Long

Michael Long is the Thomas and Susanne Murphy Professor of Neuroscience at the NYU School of Medicine. He completed his graduate studies with Barry Connors at Brown University where he investigated the role of electrical synapses in the mammalian brain. During his postdoctoral work with Michale Fee at MIT, Long began to study the songbird model system to uncover the cellular and network properties that give rise to learned vocal sequences. Since beginning his laboratory in 2010, Long has focused his attention on the neural circuits underlying skilled movements, often in the service of vocal interactions. To accomplish this, the Long lab has taken a comparative approach, examining relevant mechanisms in the songbird, a newly characterized neotropical rodent, and humans. In addition to federal funding, the Long lab has also received support from NYSCF, the Rita Allen Foundation, the Klingenstein Foundation, and the Herschel-Weill Foundation.

Long Lab

Abstract:  Vocal communication is central to our everyday lives, facilitating social exchange. Despite significant recent discoveries, the neural mechanisms underlying coordinated vocal exchanges remain poorly understood. We examine the brain processes involved in interactive vocal behaviors, focusing on forebrain circuitry in the songbird and the rodent, and we relate these to emerging human studies that employ a range of methods to manipulate and monitor cortical areas relevant for speech.