The large and vibrant Pittsburgh area yeast community meets monthly during the academic year and includes researchers from the University of Pittsburgh, the University of Pittsburgh School of Medicine, Carnegie Mellon University, and West Virginia University. Faculty, students, postdocs and research associates present their latest research discoveries using yeast as a powerful model system for performing experiments in molecular genetics, genomics, biochemistry, cell biology, evolutionary biology, and systems biology.
Participating laboratories
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https://www.biology.pitt.edu/person/jeffrey-brodsky https://www.ncbi.nlm.nih.gov/myncbi/jeffrey.brodsky.1/bibliography/public/ |
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https://scholar.google.com/citations?user=qp_jN7wAAAAJ&hl=en |
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https://www.biology.pitt.edu/person/craig-kaplan https://www.ncbi.nlm.nih.gov/myncbi/craig.kaplan.1/bibliography/public/ |
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https://labs.bio.cmu.edu/mcmanus/ https://www.ncbi.nlm.nih.gov/myncbi/charles.mcmanus.1/bibliography/public/ |
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https://www.ncbi.nlm.nih.gov/myncbi/123uoNNUaXz5-/bibliography/public/ |
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https://www.duq.edu/faculty-and-staff/jana-patton-vogt.php https://www.ncbi.nlm.nih.gov/myncbi/jana.vogt.1/bibliography/public/ |
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The Karen Arndt lab studies eukaryotic gene expression with a focus on the interplay between transcription and chromatin structure. One major area of study is the elucidation of regulatory proteins and mechanisms that control the epigenetic marking of eukaryotic genomes through histone modifications. A second major area of study is the role of chromatin structure, modification, and remodeling in regulating transcription elongation and termination. The Arndt lab uses a multi-faceted approach of genetics, genomics, proteomics, mechanistic biochemistry, and protein crosslinking experiments to address these fundamental questions in eukaryotic gene regulation. 
Work in the Jeffrey Brodsky lab focuses on understanding how misfolded proteins are recognized and destroyed in the cell, how molecular chaperones mediate protein quality control “decisions”, how cellular stress impacts protein homeostasis ("proteostasis"), and how defects in protein architecture can be corrected. Our early work contributed to the discovery of the endoplasmic reticulum associated degradation (ERAD) pathway, which we named, and ongoing studies are deciphering the mechanisms underlying this pathway in yeast, mammalian cell culture, and rodent models. The importance of ERAD is evidenced by the fact that >70 human diseases are associated with the pathway, and numerous ERAD substrates play vital roles in human physiology. 
The Nathan Clark lab studies the process of adaptive evolution, during which species adopt novel traits to overcome challenges. We retrace the evolutionary histories of genomic elements to determine the changes underlying adaptation and to discover previously unknown genetic networks. These discoveries have already led to advances in human health, species conservation, and molecular biology. To meet these goals, we have developed a suite of computational and experimental approaches employing comparative genomics. Ultimately, our research program develops an evolutionary model in which genomic elements are shaped by their co-evolution with other elements and their environment. 
The Craig Kaplan lab studies mechanisms of gene expression with a focus on RNA Polymerase II (Pol II) in the budding yeast Saccharomyces cerevisiae. We employ genetic, genomic, and biochemical approaches to understand how alterations to Pol II activity affect gene expression and cotranscriptional processes. We also are interested in mechanisms of initiation and how they may have evolved to be different while still using a conserved set of factors. 
The Joel McManus lab studies RNA regulatory control of gene expression. The lab develops and employs novel high-throughput assay systems to identify RNA cis-regulatory elements and structures, and then quantitates their impact on mRNA translation using massively parallel reporter systems. We computationally mine the resulting data to distill features and develop models that predict the functions of mRNA transcript leaders. Using these approaches, we study post-transcriptional regulation of human and fungal genes. 
Research in the Allyson O’Donnell lab focuses on the alpha-arrestins, a relatively understudied class of protein trafficking adaptor. We use the a-arrestins to define the rules that govern selective trafficking of membrane proteins in response to nutrient and stress signaling. Our lab uses cell biological, genetic, and biochemical approaches to define conserved regulatory elements that dictate selective remodeling of membrane proteomes. 
The Jana Patton Vogt lab is interested in membrane lipid biochemistry. Of particular interest is the production, transport, metabolism, and function of a class of phospholipid metabolites called glycerophosphodiesters. Glycerophosphodiesters, such as glycerophosphocholine (GPC) and glycerophosphoinositol (GPI), are produced through phospholipase B-mediated cleavage of their precursor phospholipids. My laboratory has characterized several novel genes defining this metabolism in S. cerevisiae, including a permease (Git1), a glycerophosphodiesterase (Gde1), and an acyltransferase (Gpc1). The fundamental importance of these turnover/recycling processes is illustrated by the fact that the basic components have been described in organisms spanning the biological spectrum, including pathogenic fungi and various plant species. My lab has been involved in many of those translational studies. 
The Matt Wohlever lab studies membrane protein quality control using biochemistry and structural, molecular, and cell biology. Membrane protein homeostasis (proteostasis) is a fundamental process in cell biology, but the molecular details are largely unexplored. Failures in membrane proteostasis can lead to many diseases including cancer, cardiovascular, and neurodegenerative diseases. Our key research questions are: (1) how do quality control factors discriminate between potential substrates in a complex cellular environment, including the lipid bilayer; (2) once a substrate is recognized, what are the downstream steps that lead to resolution of proteotoxic stress; and (3) how can we leverage the resulting mechanistic insights to develop therapeutic interventions in cancer and neurodegenerative diseases?