Project description:Stress responses to DNA damaging agents show characteristic responses. The effect of Azinomycin B upon cultured yeast cells in growth conditions appears to be significant. We used microarrays to detail the global programme of gene expression induced in the stress response to Azinomycin B. Keywords: stress response
Project description:DNA replication forks that are stalled by DNA damage activate an S phase checkpoint that prevents irreversible fork arrest and cell death. The increased cell death caused by DNA damage in budding yeast cells lacking the Rad53 checkpoint protein kinase is partially suppressed by deletion of the EXO1 gene. Here,we identified that loss of the histone deacetylase complex Rpd3L promotes survival of rad53∆ cells exposed to DNA damaging agents. From epistasis analysis, we show that this suppression operates in a separate pathway from the previously described suppression by deletion of EXO1.
Project description:Stress responses to DNA damaging agents show characteristic responses. The effect of Azinomycin B upon cultured yeast cells in growth conditions appears to be significant. We used microarrays to detail the global programme of gene expression induced in the stress response to Azinomycin B. Experiment Overall Design: Saccharomyces cerevisiae cells were exposed to selected doses of Azinomycin B for a period of 6 hours incubation for RNA extraction and hybridization on Affymetrix microarrays. We sought to compare stress response states of 100 and 10 ug/ml to control growth.
Project description:Treatment of cells with DNA damaging agents leads to large-scale gene expression changes. Proper transcriptional regulation is important for cells to arrest, repair damage and adjust cellular processes such as metabolism in order to survive the damaging assault. Damage-induced transcription is a highly regulated response. This study establishes a novel role for two factors, Snf1 and Rad23, in regulation of the UV-induced transcriptional response.
Project description:Telomere chromatin structure is pivotal for maintaining genome stability by regulating the binding of telomere-associated proteins and inhibition of a DNA damage response. In yeast, the silent information regulator (Sir) proteins bind to terminal telomeric repeats and to subtelomeric X-elements resulting in histone deacetylation and transcriptional silencing. Herein, we show that sir2 mutant strains display a very specific loss of a nucleosome residing in the X-element. Most yeast telomeres contain an X-element and the nucleosome occupancy defect in sir2 mutants is remarkably consistent between different telomeres.
