Project description:Investigation of whole genome gene expression level changes in C. elegans rsks-1, daf-2, daf-2 rsks-1 and daf-16; daf-2 rsks-1 mutant compared to the wild-type N2 strain. The mutants have altered longevity phenotypes. The mutants analyzed in this study are further described in Di Chen, Patrick Wai-Lun Li, Benjamin A. Goldstein, Waijiao Cai, Emma Lynn Thomas, Fen Chen, Alan E. Hubbard, Simon Melov and Pankaj Kapahi, Germline Signaling Mediates the Synergistically Prolonged Longevity by Double Mutations in daf-2 and rsks-1 in C. elegans, Cell Reports (CELL-REPORTS-D-13-00388).
Project description:Investigation of whole genome gene expression level changes in early generation Caenorhabditis elegans Bristol N2 prg-1 and Bristol N2 prg-1; daf-2 double mutant, compared to late-generation strains. A seven chip study using total RNA recovered from three separate alleles of Caenorhabditis elegans Bristol N2 prg-1 and four separate allelic combinations of a double mutant strain, Bristol N2 prg-1; daf-2 , in which prg-1 (pk2298) and prg-1 (tm872) are combined with one of three daf-2 alleles (e1368, 1370, m41).
Project description:Investigation of whole genome gene expression level changes in C. elegans rsks-1, daf-2, daf-2 rsks-1 and daf-16; daf-2 rsks-1 mutant compared to the wild-type N2 strain. The mutants have altered longevity phenotypes. The mutants analyzed in this study are further described in Di Chen, Patrick Wai-Lun Li, Benjamin A. Goldstein, Waijiao Cai, Emma Lynn Thomas, Fen Chen, Alan E. Hubbard, Simon Melov and Pankaj Kapahi, Germline Signaling Mediates the Synergistically Prolonged Longevity by Double Mutations in daf-2 and rsks-1 in C. elegans, Cell Reports (CELL-REPORTS-D-13-00388). A 47 chip study using total RNAs from C. elegans wild-type N2 (9 replicates), rsks-1 mutant (9 replicates), daf-2 mutant (9 replicates), daf-2 rsks-1 double mutant (10 replicates) and daf-16; daf-2 rsks-1 triple mutant (10 replicates) measured gene expression levels at the whole genome level.
Project description:In this experiment, steady-state mRNA levels were determined for replicated samples of N2 (wild-type reference) and fog-2(q71) homozygous mutant C. elegans. All samples were adult XX animals, which for N2 are self-fertile hermaphrodites and for fog-2(q71) spermless hermaphrodites, i.e. true females. For the fog-2 mutant animals, only those that had mated with males, and were thus gravid, were picked for RNA isolation. This ensures that all comparisons are between similar, embryo-containing animals. The experiment was motivated by the role of FOG-2 in post-transcriptional control of gene expression in germ cells, inferred from its the germline-specific phenotype of its loss and from its physical associated with the GLD-1 RNA-binding protein. Specifically, a possible role for FOG-2 in influencing mRNA stability was addressed.
Project description:Whole starved L1 larvae from four genotypes (N2, daf-2(e1370), irld-39(duk1);irld-52(duk17), and daf-2(e1370); irld-39(duk1); irld-52(duk17)) were collected after 12 hours of starvation
Project description:To exmine the role of nonsense-mediated mRNA decay process in the longevity regulation of daf-2 mutants, we sequenced transcriptomes from day 1 adult Caenorhabditis elegans: Bristol N2 (wild-type), and smg-2(qd101), daf-2(e1370) and smg-2(qd101); daf-2(e1370) mutants.
Project description:Genome maintenance defects cause complex disease phenotypes characterized by developmental failure, cancer susceptibility and premature aging. It remains poorly understood how DNA damage responses function during organismal development and maintain tissue functionality when DNA damage accumulates with aging. Here we show that the FoxO transcription factor DAF-16 is activated in response to DNA damage during development while the DNA damage responsiveness of DAF-16 declines with aging. We find that in contrast to its established role in mediating starvation arrest, DAF-16 alleviates DNA damage induced developmental arrest and even in the absence of DNA repair promotes developmental growth and enhances somatic tissue functionality. We demonstrate that the GATA transcription factor EGL-27 co-regulates DAF-16 target genes in response to DNA damage and together with DAF-16 promotes developmental growth. We propose that EGL-27/GATA activity specifies DAF-16 mediated DNA damage responses to enable developmental progression and to prolong tissue functioning when DNA damage persists.