Dr. Maria Antonietta Tosches | Tosches Lab

Abstract:

The cerebral cortex is arguably the brain area that underwent the most profound transformations in vertebrate brain evolution. The expansion of the cerebral cortex in mammals was accompanied by an explosion of neuronal diversity. To discover general principles underlying the evolution of neuron types and circuits, we study the simple cerebral cortices of non-mammalian vertebrates. Our recent work has focused on the Spanish newt Pleurodeles waltl, a species with a key phylogenetic position in the vertebrate tree. We are investigating the neuroanatomy, cell type composition, and function of the Pleurodeles brain using a combination of modern neuroscience tools.

Our work on amphibians and reptiles indicates that the cerebral cortex of ancestral tetrapods was layered, with two main classes of neurons with distinct laminar positions, molecular identities, and long-range projections. In salamanders, these two layers are generated sequentially from multipotent progenitors in an outside-in sequence. We propose that in mammals new types of pyramidal neurons evolved from these two ancestral classes by diversification, through the emergence of novel gene regulatory interactions during neuronal differentiation.

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Dr. Samantha Brugmann | Brugmann Lab

Bio:

Dr. Samantha Brugmann is a developmental biologist studying craniofacial development and disease. Her longterm goal is to help children with craniofacial anomalies by generating tissue amenable for surgical repair. To achieve this goal, her lab specifically focuses on the role the primary cilium during craniofacial development and the craniofacial anomalies that arise when the cilium do not function properly. Projects in her lab utilize avian, murine and humaninduced pluripotent stem cells to gain a better understanding of the molecular mechanisms associated with craniofacial anomalies. In addition to using existing animal models to understand human craniofacial disorders, her lab also sequences patients and generates cell-based models to uncover novel genetic causes for craniofacial ciliopathies.



Abstract:

The Brugmann Lab focuses on the understanding molecular and cellular processes important for craniofacial development and the onset of craniofacial anomalies (CFAs). CFAs represent approximately one third of all birth-defects. For the past decade, my research program has centered on treating these conditions by garnering a fundamental understanding of craniofacial development and pathological mechanisms associated with CFAs. We have specifically focused on a class of CFAs called ciliopathies, which are caused by disruptions to a cellular organelle called the primary cilium. Ciliopathies represent a fast-growing group of disorders, that can affect up to 1 in 800 people. My lab was the first to report that the craniofacial complex is the primary organ system affected in 30% of all ciliopathies, and thus coined the term craniofacial ciliopathies. My lab uses murine, avian and human model systems to understand molecular mechanisms associated with ciliopathies. Furthermore, we use these model systems to identify potential therapeutic avenues to treat this class of diseases. 

Dr. Carrie Adler | Adler Lab

Bio:

Carrie is currently an Assistant Professor in the Department of Molecular Medicine at Cornell University, where she started her lab in 2015. She attended college at Wesleyan University and afterwards worked as a technician with Bruce Mayer at Harvard Medical School, studying signal transduction pathways. For graduate school, Carrie enrolled in the Tetrad program at UCSF, joining Cori Bargmann's lab to study neural development in C. elegans. As a postdoc, Carrie trained with Alejandro Sánchez Alvarado at the University of Utah and the Stowers Institute for Medical Research.

Abstract:

Throughout our lives, we are constantly exposed to insults, including injuries, disease, and environmental toxins. Frequently referred to as a ‘fountain of youth’ given their potential for rejuvenation, stem cells have the capacity to restore damaged tissue. In most model organisms, regenerative capacity is limited and stem cells are scarce, which has made it difficult to pinpoint the mechanisms regulating their behavior. In addition, stem cell exhaustion occurs as we age, diminishing our ability to repair damaged tissues. Finally, while we have made significant progress in recapitulating organ growth in vitro, how might these tissues be used in humans to restore physiological function?

My research program has probed these questions in an emerging model organism, planarian flatworms. These animals have long been regarded as champion regenerators because they can rapidly replace any tissue that’s been damaged or lost, including the nervous system. The basis of this unlimited renewal lies in an abundant population of stem cells. My lab’s primary goals are to understand how these cells sense and respond to injury, and how they maintain genome integrity through repeated cell divisions that occur during regeneration.

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 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.

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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!



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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.

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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. 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"

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Jake Ferguson