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.

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. 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"

Watch the seminar here!

Jake Ferguson