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Aging, Metabolism, Stress, Pathogenesis, and Small RNAs in C. elegans Topic Meeting 2012 Oxygen, temperature, and food: new insights into the role of environment in C. elegans aging Matt Kaeberlein University of Washington, Department of Pathology, Seattle, WA, United States Aging is controlled by a complex interaction between environmental and genetic factors. The most studied environmental modulator of longevity is nutrient availability, with dietary restriction known to extend lifespan in species from yeast to monkeys. In addition to food, oxygen and temperature are also known to be important environmental factors in determining adult lifespan in C. elegans. Here I will describe our recent efforts to understand how each of these environmental components interacts with known genetic modifiers of aging, including insulin-like signaling, mRNA translation, and the hypoxic response. I will also describe ongoing studies to define the mechanisms of lifespan extension from stabilization of the hypoxic response transcription factor, HIF-1, under normoxic conditions. Contact: kaeber@uw.edu Lab: Kaeberlein 12 Session 2 Plenary Speaker
Contact: lapierre@burnham.org Lab: Hansen Aging, Metabolism, Stress, Pathogenesis, and Small RNAs in C. elegans Topic Meeting 2012 The transcription factor HLH-30/TFEB regulates autophagy and modulates longevity in C. elegans Louis Lapierre, Malene Hansen Sanford-Burnham Medical Research Institute The cytosolic degradation process of autophagy has emerged as a key mechanism required for lifespan extension in C. elegans, yet the underlying regulatory mechanisms remain unclear. The mammalian transcription factor TFEB was recently found to coordinately upregulate 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). In this study, we asked if the nematode ortholog of TFEB, called HLH-30, is a functional homolog of mammalian TFEB. To investigate this hypothesis, we analyzed the function of HLH-30 in long-lived, germlineless glp-1 mutants. We previously reported that glp-1 mutants display increased autophagy, and require autophagy genes to live long (Lapierre et al., Current Biology, 2012). We found that glp-1 animals, along with an increased expression of hlh-30, showed significantly elevated mRNA levels of worm orthologs for multiple TFEB autophagy and lysosomal targets. Notably, the promoters of these target genes contain conserved binding sites for HLH-30. We also observed that glp-1 animals subjected to hlh-30 RNAi showed decreased induction of targets, as well as reduced numbers of GFP::LGG-1 autophagosomal puncta, indicating that HLH-30 regulates autophagy in long-lived C. elegans. Finally, we asked if hlh-30 plays a role in longevity, as previously reported for multiple autophagy genes. We found that RNAi knockdown of hlh-30 in adult glp-1 animals significantly shortened their long lifespan, while not affecting the lifespan of wild-type animals. In addition, we observed a similar trend in another longevity model, the daf-2 insulin/IGF-1 receptor mutants, suggesting that hlh-30 plays a broader role in lifespan extension. Collectively, our findings indicate that HLH-30 is a novel longevity-modulating transcription factor, which displays functional similarity to its mammalian counterpart TFEB. Session 2 13
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