Project description:Comprehensive list of SUMO targets from the nematode Caenorhabditis elegans. SUMO conjugates isolated from transgenic worms carrying 8His and GFP tagged SUMO. The constructs rescues the lethal knock-out of a single SUMO gene, smo-1. SUMO conjugates where isolated from heat shock, arsenite exposure, and UV treated SUMO-GFP worms as well as from control non treated animals. In parallel identical purification procedure was performed with non-transgenic worms and proteins identified with this control where excluded.
Project description:This SuperSeries is composed of the following subset Series: GSE4093: Resveratrol treatment of daf-16 mutant C. elegans GSE4094: N2 worms treated with Resveratrol GSE4095: Sir-2.1 low copy transgenic Abstract: C. elegans SIR-2.1, a member of the Sir-2 family of NAD(+)-dependent protein deacetylases, has been shown to regulate nematode aging via the insulin/IGF pathway transcription factor daf-16. Treatment of C. elegans with the small molecule resveratrol, however, extends life span in a manner fully dependent upon sir-2.1, but independent of daf-16. Microarray analysis of worms treated with resveratrol demonstrates the transcriptional induction of a family of genes encoding prion-like glutamine/asparagine-rich proteins involved in endoplasmic reticulum (ER) stress response to unfolded proteins. RNA interference of abu-11, a member of this ER stress gene family, abolishes resveratrol-mediated life span extension, and overexpression of abu-11 extends the life span of transgenic animals. Furthermore, SIR-2.1 normally represses transcription of abu-11 and other ER stress gene family members, indicating that resveratrol extends life span by inhibiting sir-2.1-mediated repression of ER stress genes. Our findings demonstrate that abu-11 and other members of its ER stress gene family are positive determinants of C. elegans life span. Refer to individual Series
Project description:Transcriptional profiling of N2 vs. mir-243 worms, aiming to identify direct and indirect targets of the microRNA. N2 and mir-243 young-adult worms grown at 20C were analyzed. Three biological replicates with dye-swaps were performed.
Project description:The gas-1(fc21) mutation affects the 49 kD subunit of complex I, decreasing the rate of complex I-dependent oxidative phosphorylation. This is a model for human mitochondrial respiratory chain disease. NAD+ and PPAR-modifying drugs may confer benefits with respect to lifespan in these short-lived mutant worms. Analysis of gas-1(fc21) electron transport chain complex I mutants treated either starting in development or in young adulthood only with nicotinic acid (1 mM), resveratrol (50 microM), rosiglitazone (5 mM) or fenofibrate (14 microM) is presented. The goal is to detect transcriptional changes in clusters of genes using gene set enrichment analysis to explain treament effects in these mutant worms. Four biological replicates were performed for each treatment condition (nicotinic acid, resveratrol, rosiglitazone, and fenofibrate) for each drug beginning either in development or in young adulthood for gas-1 mutant worms, i.e., 8 treated samples in total. At most one outlier was excluded from each analysis. Untreated N2 and gas-1 in each of the control solvents (S-basal, for nicotinic acid, and 1% DMSO, for resveratrol, rosiglitazone, and fenofibrate) were also analyzed; at least 3 replicates of each were included. These were used as sources of total RNA, each for hybridization to a single Affymetrix whole-genome microarray. Analysis was performed to reveal transcriptional changes related to mutantion and/or drug treatment effects.
Project description:We aimed at investigating whether the newly identified C. elegans SPT2 histone chaperone controls chromatin structure. We decided to profile SPT-2 binding sites to identify its genomic targets and we performed GFP ChIP-seq on a C. elegans strain expressing endogenously GFP-tagged SPT-2, using WT N2 untagged worms as control for binding specificity.