Monique Stanfel

Mentors: Brian Kennedy and Peter Rabinovitch
Box: 357350
Phone: 206-616-8084
Email: mstanfel@u.washington.edu

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Studies of invertebrate aging have identified many genes in yeast and worms whose reduced expression is associated with enhanced longevity. Among the genes identified in the yeast genome-wide replicative aging screen, genes linked to the TOR signaling pathway were enriched. TOR is a central mediator of cell growth and division, monitoring nutrient availability and regulating multiple downstream events including mRNA translation, metabolism, protein homeostasis, and stress response pathways. Dr. Stanfel's project focuses on determining whether longevity pathways defined in yeast and worms are conserved in mice. Specifically, Dr. Stanfel's mouse longevity studies are focused on testing whether mutations which reduce biogenesis of 60S ribosomal subunits affect lifespan in mice. In yeast and worms, decreased abundance of 60S ribosomal subunits results in lifespan extension, and data from the Kennedy lab indicate that this pathway is related to the nutrient-sensing mechanisms of lifespan regulation which are likely conserved. Dr. Stanfel will evaluate two developed mouse models lacking genes that encode ribosomal proteins (Rpl22^-/- and Rpl29^-/-). Rpl22^-/- and Rpl29^-/- mice display translational defects, particularly decreased abundance of the 60S subunit and 80S ribosomes, respectively.