Saccharomyces cerevisiae
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA319750 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Replication-independent endogenous double-strand breaks
| PRJDB3079 | ENA
Project description:Break-chip (microarray-based double strand break mapping) analysis of mec1 cells recovering from 200 mM hydroxyurea in the presence or absence of 0.8 micromolar bathophenanthroline sulfonate (BPS). We asked if the presence of an iron chelator, BPS, during cell recovery from transient exposure to 200 mM hydroxyurea changes the global patterns of DNA double strand breaks (DSBs). We used a yeast checkpoint mutant, mec1, which has been shown to produce DSBs at replication forks after hydroxyurea was removed from the cell culture. We synchronously released cells from the G1/S transition into S phase in the presence of 200 mM hydroxyurea. After 1h treatment, the drug was removed and cells were allowed to recover in fresh medium for 1h in the presence or absence of 0.8 micromolar BPS. Recover (R) samples, R-1h-BPS and R-1h+BPS, as well as the G1 control samples were collected. Break-chip analysis was performed as previously described (Feng et al., G3(Bethesda) 2011 Oct;1(5):327-35. doi: 10.1534/g3.111.000554).
2015-01-12 | E-GEOD-64446 | biostudies-arrayexpress
Project description:Monitoring Homology Search during DNA Double-Strand Break Repair in vivo
| PRJNA192332 | ENA
Project description:Background: Chromatin remodeling complexes facilitate the access of enzymes that mediate transcription, replication or repair of DNA by modulating nucleosome position and/or composition. Ino80 is the DNA-dependent Snf2-like ATPase subunit of a complex whose nucleosome remodeling activity requires actin-related proteins, Arp4, Arp5 and Arp8, as well as two RuvB-like DNA helicase subunits. Budding yeast mutants deficient for Ino80 function are not only hypersensitive to reagents that induce DNA double strand breaks, but also to those that impair replication fork progression. Results: To understand why ino80 mutants are sensitive to agents that perturb DNA replication, we used chromatin immunoprecipitation to map the binding sites of the Ino80 chromatin remodeling complex on four budding yeast chromosomes. We found that Ino80 and Arp5 binding sites coincide with origins of DNA replication and tRNA genes. In addition, Ino80 was bound at 67% of the promoters of genes that are sensitive to ino80 mutation. When replication forks were arrested near origins in the presence of hydroxyurea (HU), the presence of the Ino80 complex at stalled forks and at unfired origins increased dramatically. Importantly, the resumption of DNA replication after release from a HU block was impaired in the absence of Ino80 activity. Mutant cells accumulated double-strand breaks as they attempted to restart replication. Consistently, ino80-deficient cells, although proficient for checkpoint activation, delay recovery from the checkpoint response. Conclusions: The Ino80 chromatin remodeling complex is enriched at stalled replication forks where it promotes the resumption of replication upon recovery from fork arrest. Keywords: ChIP-chip
2008-04-10 | GSE9420 | GEO
Project description:Integrative analysis and simulations of DNA double-strand break formation reveal cells’ heterogeneity in response to replication stress
| PRJNA577473 | ENA
Project description:Background: Chromatin remodeling complexes facilitate the access of enzymes that mediate transcription, replication or repair of DNA by modulating nucleosome position and/or composition. Ino80 is the DNA-dependent Snf2-like ATPase subunit of a complex whose nucleosome remodeling activity requires actin-related proteins, Arp4, Arp5 and Arp8, as well as two RuvB-like DNA helicase subunits. Budding yeast mutants deficient for Ino80 function are not only hypersensitive to reagents that induce DNA double strand breaks, but also to those that impair replication fork progression. Results: To understand why ino80 mutants are sensitive to agents that perturb DNA replication, we used chromatin immunoprecipitation to map the binding sites of the Ino80 chromatin remodeling complex on four budding yeast chromosomes. We found that Ino80 and Arp5 binding sites coincide with origins of DNA replication and tRNA genes. In addition, Ino80 was bound at 67% of the promoters of genes that are sensitive to ino80 mutation. When replication forks were arrested near origins in the presence of hydroxyurea (HU), the presence of the Ino80 complex at stalled forks and at unfired origins increased dramatically. Importantly, the resumption of DNA replication after release from a HU block was impaired in the absence of Ino80 activity. Mutant cells accumulated double-strand breaks as they attempted to restart replication. Consistently, ino80-deficient cells, although proficient for checkpoint activation, delay recovery from the checkpoint response. Conclusions: The Ino80 chromatin remodeling complex is enriched at stalled replication forks where it promotes the resumption of replication upon recovery from fork arrest. Keywords: ChIP-chip
2008-04-10 | GSE9233 | GEO
Project description:Meiotic DNA double strand breaks in the yeast Saccaromyces cerevisiae
| PRJNA102441 | ENA
Project description:Meiotic double-strand break end resection mapping by S1Seq
| PRJNA337955 | ENA
Project description:The Fun30 ATP-dependent nucleosome remodeler promotes resection of DNA double-strand break ends
| PRJNA168290 | ENA
Project description:Mapping of meiotic single-stranded DNA reveals double-strand break hotspots near centromeres and telomeres.
| PRJNA103295 | ENA