Under a new $3 million grant from the Glenn Foundation for Medical Research, Princeton University researchers will study the biology of aging and healthspan. Read Full Story
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Friday, October 11, 2013, 1:00 – 5:00 pm, 101 Carl Icahn Laboratory.
1:00 – 1:20 pm Coleen T. Murphy, Director - Introduction/Welcome
1:20 – 1:40 pm Gordon Berman – "Mapping the structure of behavioral senescence in Drosophila melanogaster"
1:40 – 2:00 pm Eric Klein – "Mechanical signaling in bacterial uropathogens"
2:00 – 2:20 pm Mohammad Rahimi Lenji – "Learning and memory in C. elegans: a microfluidic assay"
Amanda Crocker – "Movement towards understanding olfactory long-term memory encoding in Drosophila melanogaster"
2:20 – 2:40 pm Kevin Takasaki – "Fluorescence light-field imaging: method and applications"
2:40 – 3:00 pm Gunnar Kleemann – "Quantitative Trait Loci analysis of longevity pathways"
Dr. Monica Driscoll
Department of Molecular Biology and Biochemistry, Rutgers University "
C. elegans secrets for healthy aging: Genes, Environment, Experience, and Luck"
Design of effective therapeutic interventions that counter the deleterious aspects of aging will require a thorough definition of what actually occurs during aging at the molecular, cellular, and systems levels, as well as targeting these processes for improved maintenance. We are using the power of the C. elegans experimental model to define genes, drugs, and experiences that extend healthspan, the period of healthy life that precedes age-associated decline. In the context of a general overview on healthspan studies, I will discuss some of our recent work on changes in dendritic regrowth, synaptic deterioration, and proteostasis in aging C. elegans neurons; on the identification of microRNAs that regulate the quality of aging, one of which acts as a switch for the dietary restriction state; and on exercise contributions to late-age maintenance.
Sanford-Burnham Medical Research Institute, La Jolla, CA
October 8, 2012 1:00 pm – 2:00 pm Room 200 Carl Icahn Laboratory
Using C. elegans to understand the role of autophagy in aging
The cytosolic degradation process of autophagy plays an important role in many age-related diseases and has been directly linked to aging, including in the nematode C. elegans. However, the underlying mechanism by which autophagy modulates aging remains largely elusive. In our laboratory, we are interested in understanding how autophagy contributes to aging, and in one approach to address this question we have focused on finding conserved regulators of this process in C. elegans.
The mammalian transcription factor TFEB was recently found to coordinately up-regulate several genes involved in both the formation of the autophagosome (i.e., the vesicle sequestering material for degradation) and in lysosomal processing (i.e., compartment where active degradation takes place). We have carried out an investigation of the nematode ortholog of TFEB, called HLH-30. Our analysis indicates that HLH-30 is a novel longevity-modulating transcription factor, which displays functional similarity to its mammalian counterpart TFEB. As such, our findings accentuate a central role for autophagy in aging, and highlight the importance of transcriptional mechanisms in the regulation of autophagy.