Project description:Young adult fer-15;fem-1 Caenorhabditis elegans were infected with Staphylococcus aureus for 8 h to determine the transcriptional host response to Staphylococcus aureus. Analysis of differential gene expression in C. elegans young adults exposed to two different bacteria: E. coli strain OP50 (control), wild-type Staphylococcus aureus RN6390. Samples were analyzed at 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: response to pathogen infection, innate immunity, host-pathogen interactions
Project description:We compared animals that produce oocytes but no sperm fem-2(b245ts) to animals that produce sperm but no oocytes fem-3(q20ts). Using miRNA microarrays and we found that the mir-35-41 cluster genes were expressed to much greater extent in oogenesis than in spermatogenesis; furthermore, these miRNAs were the only C. elegans miRNAs that showed such differential germline expression.
Project description:microRNAs fine-tune the regulation of numerous biological processes by mediating gene expression post-transcriptionally. Mature miRNAs associate with argonaute (AGO) proteins to form the RNA-induced silencing complex (RISC) that binds to and blocks translation of target mRNAs. In our study, we address the function of miRNAs in regulating DNA damage responses in-vivo, by exploiting the nematode model organism Caenorhabditis elegans. Using next-generation sequencing, we obtained miRNA expression profiles of WT worms as well as mutants harboring a loss-of-function deletion of the C. elegans AGO gene alg-2 that display abnormal cell death in response to genotoxic stress. 2.5 hours after exposure to ionizing irradiation, the miRNA transcriptomes of both WT and alg-2(ok304) mutant worms were only mildly altered in comparison to their respective untreated controls. However, irrespective of treatment, alg-2(ok304) mutants exhibited noticeable dysregulation of several miRNA families with known physiological functions. Reduced levels of some of these miRNAs might explain the abnormal DNA damage response of alg-2-deficient C. elegans.
