Saccharomyces cerevisiae
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA262013 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Eukaryotic DNA replication initiates from multiple sites on each chromosome called replication origins. In the budding yeast Saccharomyces cerevisiae, origins are defined at discrete sites. Regular spacing and diverse firing characteristics of origins are thought to be required for efficient completion of replication, especially in the presence of replication stress. However, a S. cerevisiae chromosome III harboring multiple origin deletions has been reported to replicate relatively normally, and yet how an origin-deficient chromosome could accomplish successful replication remains unkown. To address this issue, we deleted seven well-characterized origins from chromosome VI, and found that thsese deletions do not cause gross growth defects even in the presence of replication inhibitors. We demonstrated that the origin deletions do cause a strong decrease in the binding of the origin recognition complex. Unexpectedly, replication profiling of this chromosome showed that DNA replication initiates from non-canonical loci around deleted origins in yeast. These results suggest that replication initiation can be unexpectedly flexible in this organism.
2014-09-26 | GSE61743 | GEO
Project description:Mammalian chromosome replication starts from distinct sites, but the principles governing initiation site selection are unclear because proteins essential for DNA replication do not exhibit sequence-specific DNA binding. We identified a replication initiation determinant (RepID) protein that binds a subset of replication initiation sites. A large fraction of RepID binding sites share a common G-rich motif and exhibit elevated replication initiation. RepID is required for initiation of DNA replication from Rep-ID bound replication origins, including the origin at the human beta-globin (HBB) locus. At HBB, RepID is involved in an interaction between the replication origin (Rep-P) and the locus control region. RepID depleted murine embryonic fibroblasts exhibit abnormal replication fork progression and fewer replication initiation events. These observations are consistent with a model suggesting that RepID facilitates replication initiation at a distinct group of human replication origins.
2016-06-02 | GSE80298 | GEO
Project description:Mammalian chromosome replication starts from distinct sites, but the principles governing initiation site selection are unclear because proteins essential for DNA replication do not exhibit sequence-specific DNA binding. We identified a replication initiation determinant (RepID) protein that binds a subset of replication initiation sites. A large fraction of RepID binding sites share a common G-rich motif and exhibit elevated replication initiation. RepID is required for initiation of DNA replication from Rep-ID bound replication origins, including the origin at the human beta-globin (HBB) locus. At HBB, RepID is involved in an interaction between the replication origin (Rep-P) and the locus control region. RepID depleted murine embryonic fibroblasts exhibit abnormal replication fork progression and fewer replication initiation events. These observations are consistent with a model suggesting that RepID facilitates replication initiation at a distinct group of human replication origins. Nascent strands were purified with the lambda exonuclease methods from HCT116 cells and sequenced. Chromatin from unsyncrhonized untreated cultures of U2OS cells was subjected to ChIP-Seq with antibody directed against RepID/PHIP
2016-06-02 | E-GEOD-80298 | biostudies-arrayexpress
Project description:Eukaryotic DNA replication initiates from multiple sites on each chromosome called replication origins. In the budding yeast Saccharomyces cerevisiae, origins are defined at discrete sites. Regular spacing and diverse firing characteristics of origins are thought to be required for efficient completion of replication, especially in the presence of replication stress. However, a S. cerevisiae chromosome III harboring multiple origin deletions has been reported to replicate relatively normally, and yet how an origin-deficient chromosome could accomplish successful replication remains unkown. To address this issue, we deleted seven well-characterized origins from chromosome VI, and found that thsese deletions do not cause gross growth defects even in the presence of replication inhibitors. We demonstrated that the origin deletions do cause a strong decrease in the binding of the origin recognition complex. Unexpectedly, replication profiling of this chromosome showed that DNA replication initiates from non-canonical loci around deleted origins in yeast. These results suggest that replication initiation can be unexpectedly flexible in this organism. In this study, we aimed to establish an independent system to investigate how an origin-deficient chromosome is replicated. To this end, we systematically deleted seven well-characterized origins on the left arm of S. cerevisiae chromosome VI and analyzed (1) Orc2 localization during G2/M arrest and (2) BrdU incorporation during synchronous release from G1 arrest into S-phase, and compared the results to wild-type cell signals. For Orc2 ChIP-Chip experiments, Orc-bound DNA was isolated from Orc2-2Xlinker-3XFlag epitope-tagged cells arrested in G2/M using antibodies against Flag. For BrdU ChIP-Chip experiments, actively replicating DNA was isolated from cells harboring a single integrated BrdU incorporation vector released synchronously into 200mM HU using antibodies against BrdU. Immunoprecipitated and input (Orc2) or G1 (BrdU) DNA was then amplified and competitively hybridized to high-resolution strand-specific microarrays covering chromosomes III, VI, and XII.
2014-09-26 | E-GEOD-61743 | biostudies-arrayexpress
Project description:In this study, we map sites of replication initiation and breakage in primary cells at high resolution under conditions of replication stress. We show that replication initiates between transcribed genes within nucleosome-depleted structures established by long asymmetrical poly(dA:dT) tracts flanking the initiation site. Paradoxically, large (>20 bp) homopolymeric (dA/dT) tracts are also preferential sites of polar replication fork stalling and collapse. We propose that the evolutionary expansion of poly(dA:dT) tracts in eukaryotic genomes serves to promote replication initiation, but at the cost of increasing chromosome fragility.
2018-08-01 | GSE116320 | GEO
Project description:In this study, we map sites of replication initiation and breakage in primary cells at high resolution under conditions of replication stress. We show that replication initiates between transcribed genes within nucleosome-depleted structures established by long asymmetrical poly(dA:dT) tracts flanking the initiation site. Paradoxically, large (>20 bp) homopolymeric (dA/dT) tracts are also preferential sites of polar replication fork stalling and collapse. We propose that the evolutionary expansion of poly(dA:dT) tracts in eukaryotic genomes serves to promote replication initiation, but at the cost of increasing chromosome fragility.
2018-08-01 | GSE116319 | GEO
Project description:In this study, we map sites of replication initiation and breakage in primary cells at high resolution under conditions of replication stress. We show that replication initiates between transcribed genes within nucleosome-depleted structures established by long asymmetrical poly(dA:dT) tracts flanking the initiation site. Paradoxically, large (>20 bp) homopolymeric (dA/dT) tracts are also preferential sites of polar replication fork stalling and collapse. We propose that the evolutionary expansion of poly(dA:dT) tracts in eukaryotic genomes serves to promote replication initiation, but at the cost of increasing chromosome fragility.
2018-08-01 | GSE116318 | GEO
Project description:In this study, we map sites of replication initiation and breakage in primary cells at high resolution under conditions of replication stress. We show that replication initiates between transcribed genes within nucleosome-depleted structures established by long asymmetrical poly(dA:dT) tracts flanking the initiation site. Paradoxically, large (>20 bp) homopolymeric (dA/dT) tracts are also preferential sites of polar replication fork stalling and collapse. We propose that the evolutionary expansion of poly(dA:dT) tracts in eukaryotic genomes serves to promote replication initiation, but at the cost of increasing chromosome fragility.
2018-08-01 | GSE116317 | GEO
Project description:In this study, we map sites of replication initiation and breakage in primary cells at high resolution under conditions of replication stress. We show that replication initiates between transcribed genes within nucleosome-depleted structures established by long asymmetrical poly(dA:dT) tracts flanking the initiation site. Paradoxically, large (>20 bp) homopolymeric (dA/dT) tracts are also preferential sites of polar replication fork stalling and collapse. We propose that the evolutionary expansion of poly(dA:dT) tracts in eukaryotic genomes serves to promote replication initiation, but at the cost of increasing chromosome fragility.
2018-08-01 | GSE116316 | GEO
Project description:In this study, we map sites of replication initiation and breakage in primary cells at high resolution under conditions of replication stress. We show that replication initiates between transcribed genes within nucleosome-depleted structures established by long asymmetrical poly(dA:dT) tracts flanking the initiation site. Paradoxically, large (>20 bp) homopolymeric (dA/dT) tracts are also preferential sites of polar replication fork stalling and collapse. We propose that the evolutionary expansion of poly(dA:dT) tracts in eukaryotic genomes serves to promote replication initiation, but at the cost of increasing chromosome fragility.
2018-08-01 | GSE116315 | GEO