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Dynamics of replication-independent histone turnover in budding yeast

ABSTRACT: Dynamics of replication-independent histone turnover in budding yeast

PROVIDER: PRJNA99055 | ENA |

REPOSITORIES: ENA

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Dynamics of replication-independent histone turnover in budding yeast

Project description:This SuperSeries is composed of the following subset Series: GSE6664: Ratios for unsync cells GSE6665: Ratios for G1 arrested cells (Printed array) GSE6666: Ratios for G1 arrested cells (Agilent array) GSE6667: PolII occupancy GSE6668: Nucleosome occupancy GSE6669: H3 occupancy GSE6670: Ratios for Htz1D cells (Agilent array) Keywords: SuperSeries Refer to individual Series

2010-06-11 | E-GEOD-6680 | biostudies-arrayexpress

Dynamics of replication-independent histone turnover in budding yeast

Project description:This SuperSeries is composed of the SubSeries listed below.

2007-05-16 | GSE6680 | GEO

Replication-independent histone turnover confers regulatory genome for adult heart homeostasis

Project description:Replication-independent histone turnover confers regulatory genome for adult heart homeostasis

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Replication-independent histone turnover confers regulatory genome for adult heart homeostasis [Mnase-Seq]

Project description:Disruption and replacement of nucleosomal histone (histone turnover, HT) take place during transcription and cell division. Here we examined the functional roles for replication-independent HT in directing precise regulatory genome in terminally differentiated cardiomyocytes (CMs) of adult heart. Surprisingly, histone H2B pausing and chasing assay revealed the histone halftime ~2.5 weeks in non-replicating CMs, in sharp contrast to the longer halftime of CMs, despite in the abscence of replication-dependent passive dilution of labeled histones. Regions of high HT identified enhancers of important heart function. Co-occupancy of mutiple cardiac transcription factors in part accounted for enhancers on sites lacking nucleosome eviction by passage of RNA polymerase II. Unexpectedly, both polycomb EED and HDACs augmented HT rate in bufferring poised enhancer activition without alteration of nucleosome occupancy. Thus, our results suggest replication-indenpendent HT as an additional layer of chromatin-based regulation of functional homeostasis.

2019-06-14 | GSE103680 | GEO

Replication-independent histone turnover confers regulatory genome for adult heart homeostasis [ChIP-Seq]

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Genome-wide analysis reveals that budding yeast Rif1 binds to replication origins and at blocked replication forks to protect nascent DNA

Project description:This experiment details ChIP sequencing to decipher the binding sites of the Rif1 protein in budding yeast. Rif1 binds most strongly to telomeres where its binding is mediated by Rap1. To reduce telomere binding and help reveal Rap1-independent binding sites, a truncation mutant of Rif1 lacking the Rap1 interaction domain was constructed and analysed. Binding was examined at various cell-cycle stages to elucidate the role of Rif1 in DNA replication and other chromosome transactions.

2018-12-31 | E-MTAB-6736 | biostudies-arrayexpress

Rif1 acts through Protein Phosphatase 1 and independent of replication timing to suppresses telomere extension in budding yeast

Project description:Rif1 acts through Protein Phosphatase 1 and independent of replication timing to suppresses telomere extension in budding yeast

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Rif1 acts through Protein Phosphatase 1 and independent of replication timing to suppresses telomere extension in budding yeast

Project description:The Rif1 protein negatively regulates telomeric TG repeat length in the budding yeast S. cerevisiae, but how it prevents telomere over-extension is unknown. Rif1 was recently shown to control DNA replication by acting as a Protein Phosphatase 1 (PP1)-targeting subunit. Therefore we investigated whether Rif1 controls telomere length by targeting PP1 activity. We find that a Rif1 mutant that cannot interact with PP1 causes a long-telomere phenotype, similar to that of rif1∆ cells. Compromised PP1 function also causes telomere extension. Tethering PP1 at a specific telomere partially substitutes for Rif1 in limiting TG repeat length, confirming the importance of PP1 in telomere length control. Ablating Rif1-PP1 interaction leads to precocious activation of telomere-proximal replication origins and aberrantly early telomere replication. However, we find that Rif1 still limits telomere length even if nearby replication origins are deleted, indicating that effects of Rif1 on telomere length are not mediated through replication timing. Instead we find that, even at a telomere created after DNA synthesis during a mitotic block, Rif1-PP1 interaction is required to suppress telomere lengthening and prevent inappropriate recruitment of Tel1 kinase. Overall, our results show that Rif1 controls telomere length by recruiting PP1 to directly suppress telomerase-mediated TG repeat lengthening.

2018-02-14 | GSE109241 | GEO

Genome-wide incorporation dynamics reveal distinct categories of turnover for the histone variant H3.3

Project description:We developed a system to study the DNA replication-independent turnover nucleosomes containing the histone variant H3.3 in mammalian cells. By measuring the genome-wide incorporation of H3.3 at different time points following epitope-tagged H3.3 expression, we find three categories of H3.3-nucleosome turnover in vivo: rapid turnover, intermediate turnover and, specifically at telomeres, slow turnover. Our data indicate that H3.3-containing nucleosomes at enhancers and promoters undergo a rapid turnover that is associated with active histone modification marks including H3K4me1, H3K4me3, H3K9ac, H3K27ac and the histone variant H2A.Z. The rate of turnover is negatively correlated with H3K27me3 at regulatory regions and with H3K36me3 at gene bodies. Examination of incorporation dynamics of histone variant H3.3

2013-10-23 | E-GEOD-51505 | biostudies-arrayexpress

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