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Aging, Metabolism, Stress, Pathogenesis, and Small RNAs in C. elegans Topic Meeting 2012 Identification of DAF-16 Co-regulators with Tandem Affinity Purification and MudPIT Thomas Heimbucher 1 , Zheng Liu 1 , Andrea Carrano 1 , Carine Bossard 1 , Bryan Fonslow 2 , Jonathan Yates 2 , Tony Hunter 1 , Andrew Dillin 1 1 The Salk Institute for Biological Studies, La Jolla, CA, USA, Howard Hughes Medical Institute, Glenn Center for Aging Research, 2 The Scripps Research Institute, La Jolla, CA The FoxO transcription factor DAF-16 regulates a wide range of organismal functions: it is involved in C. elegans development and reproduction, in stress response and life span regulation. Association of DAF-16 with diverse binding partners might be crucial for mediating these heterogeneous functions. To identify DAF-16 regulators we established a biochemical approach to purify DAF-16 associated proteins. DAF-16 was fused to various epitop-tags. On the basis of a reporter assay it was analyzed whether tagged DAF-16 versions were transcriptionally active. Their activity was further assessed by their ability to rescue phenotypes of a daf-16 null mutant. A functional tagged DAF-16 variant was used to generate a transgenic worm line. DAF-16 protein complexes were isolated by tandem affinity purification and potential DAF-16 binding partners were identified by tandem mass-spectrometry (MudPIT). In an additional reporter based screen DAF-16 co-regulators were validated. Their potential roles in dauer formation, stress resistance and longevity are currently being pursued. We will discuss their identity and potential functions in insulin/IGF-1 signaling. This work was supported in part by the Austrian Science Fund (FWF, grant J2734), by a grant from NIH, and by the Glenn Center for Aging Research. Contact: theimbucher@salk.edu Lab: Dillin 18 Session 3
Contact: emilie.demoinet@mcgill.ca Lab: Roy Aging, Metabolism, Stress, Pathogenesis, and Small RNAs in C. elegans Topic Meeting 2012 AMPK regulates a novel UPR-like response to mediate survival during nutrient stress in C. elegans Emilie Demoinet, Julie Mantovani, Richard Roy McGill University, Montreal, Canada To enhance survival during periods of prolonged nutrient stress, many organisms execute developmental or reproductive diapause, which are reversible states of developmental dormancy. When growth conditions are suboptimal, Caenorhabditis elegans can arrest its development and execute a diapause like state. The best characterized of these are the first larval stage (L1) and dauer diapause. The C. elegans L1 arrest is a response to an insufficient level of nutrient to initiate postembryonic development, whereby development is suspended and environmental stress resistance is increased without obvious morphological modification. Wild type L1 hatchlings can normally survive up to 2 weeks in the absence of food under these conditions. We have shown that maximal survival in the L1 diapause requires aak-2, one of the 2 homologues of the alpha subunit of AMP-activated protein kinase (AMPK). AMPK is a metabolic master switch that is activated in response to various nutritional and stress signals. Its main function is to maintain cellular energy homeostasis by enhancing energy generating pathways, while blocking energy-consuming processes. We found that larvae that lack AMPK (aak(0)), are compromised for protein folding allowing aggregates to accumulate in the L1 larvae, leading to their premature death after 5 days. The addition of glucose, delays aggregate accumulation and partially rescues survival. A similar accumulation of unfolded protein is observed in starved wild type L1 larvae just prior to death, which is delayed following glucose addition, while increasing their survival twofold. Accumulation of misfolded protein activates a highly conserved adaptive signaling cascade known as the unfolded protein response (UPR), which, when activated, can lead to adaptation or death. We have found that in the presence of an energetic stress, a previously uncharacterized UPR-like response involving novel effectors becomes activated to ensure organismal survival. Based on genetic and cell biological data, we suggest that AMPK regulates this response to prolong survival in the diapause until favorable energy conditions are restored. Session 3 19
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