Saccharomyces cerevisiae
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA268316 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1661353.fastq.gz | Fastqsanger.gz | |||
| SRR1661354.fastq.gz | Fastqsanger.gz | |||
| SRR1661355.fastq.gz | Fastqsanger.gz | |||
| SRR1661356.fastq.gz | Fastqsanger.gz | |||
| SRR1661357.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Dynamics of nucleosome positioning maturation following genomic replication
| PRJNA315674 | ENA
Project description:We have previously shown that Okazaki fragments in Saccharomyces cerevisiae are sized according to the chromatin repeat. Here we demonstrate that nucleosome positioning is rapidly established on newly synthesized DNA. Using deep sequencing, we demonstrate that ATP-dependent chromatin remodeling enzymes, Isw1 and Chd1, collaborate with histone chaperones, such as CAF-1 and Rtt106, to remodel nucleosomes, as they are loaded. Importantly, we find that nucleosome positioning is ultimately specified by select sequence-specific DNA-binding factors, which serve as physical cues for chromatin remodeling. Our results provide a mechanistic understanding of how chromatin structures are replicated in vivo, and show that chromatin structure at gene promoters is rapidly established after DNA replication. Altogether, our data provide evidence for coordinated âloading and remodelingâ of nucleosomes behind the replication fork, in collaboration with packing of nucleosomes against a barrier. 7 samples, including a wild type, are included. All are single-end sequenced via Ion Torrent PGM methodology.
2016-04-14 | E-GEOD-63583 | biostudies-arrayexpress
Project description:We have previously shown that Okazaki fragments in Saccharomyces cerevisiae are sized according to the chromatin repeat. Here we demonstrate that nucleosome positioning is rapidly established on newly synthesized DNA. Using deep sequencing, we demonstrate that ATP-dependent chromatin remodeling enzymes, Isw1 and Chd1, collaborate with histone chaperones, such as CAF-1 and Rtt106, to remodel nucleosomes, as they are loaded. Importantly, we find that nucleosome positioning is ultimately specified by select sequence-specific DNA-binding factors, which serve as physical cues for chromatin remodeling. Our results provide a mechanistic understanding of how chromatin structures are replicated in vivo, and show that chromatin structure at gene promoters is rapidly established after DNA replication. Altogether, our data provide evidence for coordinated “loading and remodeling” of nucleosomes behind the replication fork, in collaboration with packing of nucleosomes against a barrier.
2016-04-14 | GSE63583 | GEO
Project description:Numerous nucleosome remodeling enzymes tightly regulate nucleosome positions in eukaryotic cells. Transcription and statistical positioning of nucleosomes may also contribute to proper nucleosome organization. Individual contributions remain controversial due to strong redundancy of processes acting on the nucleosome landscape. By incisive yeast genome engineering we radically decreased their redundancy. We find the transcriptional machinery to be disruptive of evenly spaced nucleosomes, and proper nucleosome density critical for their biogenesis. INO80 spaces nucleosomes in vivo and positions the first nucleosome covering genes. It requires its Arp8 and Ies2 subunits, but unexpectedly not the Nhp10 module, for spacing. Whereas H2A.Z stimulates INO80 in vitro, its presence is dispensable for INO80 +1 positioning function in vivo. DNA damage, recombination and transposon integration assays suggest that evenly spaced nucleosomes protect cells against genotoxic stress. We derive a unifying model of the biogenesis of the nucleosome landscape and suggest that it evolved not only to regulate but also to protect the genome.
2021-10-20 | GSE141007 | GEO
Project description:The positioning of nucleosomes within the coding regions of eukaryotic genes is aligned with respect to transcriptional start sites. This organization is likely to influence many genetic processes, requiring access to the underlying DNA. Here we show that the combined action of Isw1 and Chd1 nucleosome spacing enzymes is required to maintain this organization. In the absence of these enzymes regular positioning of the majority of nucleosomes is lost. Exceptions include the region upstream of the promoter, the +1 nucleosome and a subset of locations distributed throughout coding regions where other factors are likely to be involved. These observations indicated that ATP-dependent remodeling enzymes are responsible for directing the positioning of the majority of nucleosomes within the Saccharomyces cerevisiae genome. Examination of nucleosome positioning in mutants of snf2-related enzymes Other data used in this study are provided in GEO Series GSE31301 and GSE31833.
2011-09-16 | E-GEOD-31015 | biostudies-arrayexpress
Project description:A role of RPA in replication coupled nucleosome assembly
| PRJNA326595 | 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: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