GSE67150
Characterization of H3 density, H3 or H4 acetylation, Rpd3 binding, TFIIB binding, and Rpb3 (pol II) binding in wild type and rpd3 cells as they transition from logarithmic growth to diauxic shift to quiescence [ChIP-Seq]
Binding profiles for H3 and H4ac were determined as cells transition from log growth to quiescence. We found that massive chromatin changes that reflect global transcriptional repression occur after the diauxic shift in an Rpd3-dependent manner.  Binding of Rpd3 is dramatically expanded to reflect binding at thousands of genes after quiescence entry, demonstrating an Rpd3-driven mechanism to change chromatin and repress transcription after entry into quiescence. Overall design: Chomatin was harvested and fragmented from cells during log growth, after the diauxic shift, and after quiescence entry.  H3 ChIP, H4 hyperacetyl ChIP, H3K23ac ChIP, Rpd3-Myc ChIP, Rpb3 (pol II) ChIP, or TFIIB ChIP was performed to monitor genomic distribution at different times in wild type or rpd3 (H3 or H4ac) strains.