Dr. Francois Spitz | Spitz Lab

Bio:
PhD from Université Paris 6 (France)
Group Leader at the European Molecular Biology Laboratory (2006-2015) (Heidelberg, Germany)
Head of Research Unit at the Institut Pasteur (2015-2019) (Paris, France)
Professor, The University of Chicago (2019-.)

Abstract:
The mechanisms that regulate the efficiency and specificity of interactions between distant genes and cis-regulatory elements such as enhancers play a central role in shaping the specific regulatory programs that control cell fate and identity. In particular, the (epi)genetic elements that organize the 3D folding of the genome in specific loops and domains have emerged as key determinants of this process. I will discuss our current views on how 3D genome architecture is organized, how it influences gene regulatory interactions and illustrate how alterations of the mechanisms and elements that organize genomes in 3D could contribute to genomic disorders and genome evolution.

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. 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.