Project description:Reproductive cessation is perhaps the earliest aging phenotypes humans experience. Similarly, C. elegans' reproduction ceases in mid-adulthood. Although somatic aging has been studied in both worms and humans, mechanisms regulating reproductive aging are not yet understood. Here we show that TGF-beta Sma/Mab activity regulates reproductive aging transcriptionally separable from its regulation of body size growth. This SuperSeries is composed of the following subset Series: GSE23446: Reproductive aging: sma-2;fem-1 day 8 oocyte vs fem-1 day 8 oocyte GSE23447: Reproductive aging: fem-1 day 3 oocyte vs fem-1 day 8 oocyte GSE23448: Body size regulation and TGF-beta Sma/Mab pathway: sma L4 vs N2 L4 Refer to individual Series
Project description:To find genes in C. elegans oocytes associated with reproductive aging. Five replicates comparing RNA from oocyte samples collected from day 3 fem-1(hc17) animals with RNA from oocyte samples collected from day 8 fem-1(hc17) animals. Three out of five are dye-flipped.
Project description:To find genes downstream of the TGF-beta Sma/Mab pathway in C. elegans oocytes associated with reproductive aging. Eight replicates comparing RNA from oocyte samples collected from day 8 sma-2(e502);fem-1(hc17) animals with RNA from oocyte samples collected from day 8 fem-1(hc17) animals. Five out of eight are dye-flipped.
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
