Dr. Carol Baskin 

Abstract:
What controls the timing of seed germination in nature? This question is of much interest because the timing of seed dormancy-break and germination are an important part of the adaptation of a species to its habitat. Thus, we want to know what environmental conditions are required for seed dormancy-break and germination in various kinds of habitats from the tropics to the arctic, i.e. germination ecology.

My first germination experiments were conducted in 1966 when I was a graduate student at Vanderbilt University; I am still expanding my knowledge about seeds of wild plants. My original work/interests have expanded from germination ecology to the world biogeography of nondormancy and of the five classes/kinds of dormancy and to the evolutionary relationships of nondormancy and the classes of dormancy.

I have studied ca. 400 species from Kentucky/Tennessee, as well as species from Hawaii, Tiawan and Sweden. With collaborators, I have been involved in seed germination studies in Argentina, Australia, Brazil, China, India, Iran and Japan. The world biogeography of seed dormancy was part of a book entitled “Seeds: ecology, biogeography, and evolution of dormancy and germination, C.C. Baskin and J.M. Baskin, 1998 (1^st ed.) 2014 (2^nd ed.), Elsevier/Academic Press,” which contained a complication of data on the world biogeography of seed dormancy for ca. 3,000 (1^st ed.) and 13, 600 (2^nd ed.) species. This data set provides an overview of seed dormancy of trees, shrubs and herbs in all the major vegetation zones on earth, and it has now been used by various collaborators to help investigate other aspects of seed biology, including the evolution of seed dormancy (i.e. dormancy transition states).  

I am a plant ecologist, and as such I seek information about the fossils and palaeohistory of seeds, embryo morphology, dormancy-breaking and germination requirements of seeds of species in all the major vegetation zones on earth and evolutionary relationships of nondormancy and the five classes of dormancy. Recently, I have been exploring how palaeohistory, biogeography and phylogeny have influenced seed dormancy-breaking and germination requirements in highly species-rich families such as the Asteraceae (ca. 30,000 species, sunflower family), Myrtaceae (ca. 6,000, Eucalyptus family) and Rubiaceae (ca. 13, 460 species, coffee family).

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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. Tara Smiley | Smiley Lab

Bio:
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. 

Abstract: 
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.

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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. 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. 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!