Seminars

Peng Li, Professor, School of Life Sciences, Tsinghua University

Lipid droplets (LDs) are dynamic sub-cellular organelles that store neutral lipids and play vital roles in metabolic homeostasis. Dysfunctional LD biogenesis or growth leads to disorders including obesity, fatty liver disease, diabetes, and atherosclerosis. We identified CIDE family proteins including CIDEA, CIDEB, and CIDEC as crucial factors in controlling LD growth through an LD fusion process. During this process, CIDE proteins are enriched at LD-LD contact sites through gel-like phase separation, which generates highly plastic fusion plates with unique lipid passageways for lipid transfer, leading to LD fusion. Importantly, we are able to reconstitute CIDEC-mediated LD fusion in vitro and identified PI4P as a specific factor to recruit CIDEC to LD surface. In addition, CLSTN3β, by localizing to ER-LD contact sites, inhibits CIDE proteins-mediated LD fusion, contributing to multilocular LD formation and promoting lipid utilization in brown adipocytes. Besides CIDE proteins, we will discuss various other regulatory factors in controlling LD dynamics and its interaction with other sub-cellular organelles. An-imaging based method in measuring lipolysis rate at a single LD level will also be described.

Speaker: Jae Myoung Suh, Associate Professor, KAIST (Korea Advanced Institute of Science and Technology)

Adipose tissue functions as both an energy reservoir and an endocrine organ, requiring precise coordination to maintain metabolic health. Our studies identify the transcriptional coregulators YAP/TAZ, downstream effectors of the Hippo signaling pathway, as key regulators coordinating these distinct functions. Using a mouse model with adipocyte-specific YAP/TAZ activation, we demonstrate that YAP/TAZ drive dramatic remodeling of adipose tissue, characterized by the dedifferentiation of mature adipocytes into lipid-depleted, progenitor-like cells. Surprisingly, despite marked reduction in fat mass, these mice are protected from the metabolic perturbations typically associated with lipodystrophy. This protection is mediated by paradoxically elevated circulating leptin levels, which enhance systemic energy expenditure through increased fat oxidation. Mechanistically, YAP/TAZ regulate adipocyte function through two distinct transcriptional pathways: suppression of PPARγ target genes via a YAP/TAZ-PPARγ axis, and upregulation of leptin expression through a YAP/TAZ-TEAD axis acting at an upstream enhancer element of the Lep gene. Furthermore, we find that YAP/TAZ activity is both correlated with and required for leptin regulation in response to fasting and feeding states. These findings extend our understanding of the Hippo-YAP/TAZ pathway beyond its canonical role in organ size control, revealing its critical function in integrating adipose tissue plasticity with systemic energy homeostasis.

Speaker: Livleen Gill, MBA, RDN, LDN, FAND
President of the Academy of Nutrition and Dietetics

Livleen Gill is President and CEO of Apostle Group LLC, as well as CEO of the Wholesome Village Inc. Livleen is a graduate of Punjab University in India and earned a graduate degree from Punjabi University. She completed her coordinated program in dietetics at Buffalo State University and Howard University. Livleen earned an MBA from the University of Maryland – University College.

Noah Whiteman is Professor of Genetics, Genomics, Evolution and Development in the Department of Molecular & Cell Biology and the Department of Integrative Biology at UC Berkeley. His new book is Most Delicious Poison: The Story of Nature's Toxins—From Spices to Vices, published in 2023. Professor Whiteman will be speaking about his book and research, followed by a conversation with Professor Michael Silver and audience Q&A.

Speaker: Renata Pereira Alambert, Assistant Professor, The University of Iowa

Seminar details to come.

Speaker: Gary Siuzdak, Professor, Scripps Research

The metabolome and lipidome are a collection of small-molecule chemical entities involved in metabolism, that have traditionally been studied with the aim of identifying biomarkers in the diagnosis and prediction of disease progression. However, the value of metabolomics/lipidomics has been redefined from a simple biomarker identification tool to a technology leading to the discovery of active drivers of biological processes. I will discuss how we have developed and applied these technologies to discover new biologically active endogenous metabolites and lipids that impact human health.

Speaker: Lene Juel Rasmussen, Professor, University of Copenhagen, Denmark

The pursuit of understanding the molecular mechanisms underlying human longevity has emerged as a central focus in biomedical research, driven by the challenges posed by an aging global population. In this presentation, I will explore recent advancements in the identification and characterization of human longevity genes, shedding light on the complex interplay between genetic factors and lifespan regulation.

The discussion will center on the functional analysis of a newly discovered longevity gene OSER1. Our findings provide valuable insights into the gene's role in fundamental cellular processes, including oxidative stress response, cellular senescence, and mitochondrial function. Additionally, I will highlight the potential therapeutic implications of this research, emphasizing innovative strategies and interventions designed to modulate the expression or activity of longevity genes. These approaches hold promise for promoting healthy aging and delaying the onset of age-related diseases.

Speaker: Mark O. Huising, Professor, University of California, Davis

Dr. Huising is a Professor at the University of California Davis where he leads a lab focused on the important role of intra-islet feedback on the regulation of islet fate and function. He completed his formal undergraduate and graduate education in his native the Netherlands after moving to California to train as a postdoctoral fellow at the Salk Institute with Wylie Vale. It was there that he laid the foundation for his current research program that has focused on local crosstalk between different endocrine cells in pancreatic islets. Mark discovered the function of the peptide hormone Ucn3 as the principal paracrine factor to activate pancreatic delta cells – feedback that determines the glucose setpoint in vivo. This discovery has led to a broad focus on pancreatic delta cells and their physiological contribution to glucose homeostasis in response to a variety of physiological and metabolic cues including ghrelin and ligands for the FFAR4 fatty acid receptor. In a separate line of research, Mark discovered an entirely new beta cell type that lacks key maturity markers including Ucn3 and Glut2 that had gone unnoticed for decades. This discovery highlights the heterogeneity that exists among beta cells that betrays beta cell plasticity that is amplified under conditions of beta cell stress during diabetes. Research from Mark's lab uses a combination of carefully validated mouse models with sophisticated live imaging experiment to observe the kinetics of multiple signaling cascades directly in intact islets in real time to quantify the changes in signaling dynamics that underly the regulation of insulin and glucagon release. Mark is an AAAS fellow, a UC Davis Chancellor's fellow and the recipient of a 2023 UC Davis Graduate Mentoring Award. Mark has dedicated his service commitment to climate advocacy on the University of California Davis campus and beyond, for which he was awarded the 2021 UC Davis Faculty Sustainability Champion.