Histone deacetylation promotes transcriptional silencing at facultative heterochromatin
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ABSTRACT:
PROVIDER: PRJNA428233 | ENA |
REPOSITORIES: ENA
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Project description:It is important to accurately regulate the expression of genes involved in development and environmental response. In the fission yeast Schizosaccharomyces pombe, meiotic genes are tightly repressed during vegetative growth. Despite being embedded in heterochromatin these genes are transcribed and believed to be repressed primarily at the level of RNA. However, the mechanism of facultative heterochromatin formation and the interplay with transcription regulation is not understood. We show genome-wide that HDAC-dependent histone deacetylation is a major determinant in transcriptional silencing of facultative heterochromatin domains. Indeed, mutation of class I/II HDACs leads to increased transcription of meiotic genes and accumulation of their mRNAs. Mechanistic dissection of the pho1 gene where, in response to phosphate, transient facultative heterochromatin is established by overlapping lncRNA transcription shows that the Clr3 HDAC contributes to silencing independently of SHREC, but in an lncRNA-dependent manner. We propose that HDACs promote facultative heterochromatin by establishing alternative transcriptional silencing.
2018-03-19 | GSE108668 | GEO
Project description: Not available
| S-EPMC6009587 | biostudies-literature
Project description:We found PEAT complexes mediate histone deacetylation and heterochromatin condensation and thereby facilitate heterochromatin silencing.
2018-06-21 | GSE116066 | GEO
Project description:We found PEAT complexes mediate histone deacetylation and heterochromatin condensation and thereby facilitate heterochromatin silencing.
2018-06-21 | GSE116065 | GEO
Project description:We found PEAT complexes mediate histone deacetylation and heterochromatin condensation and thereby facilitate heterochromatin silencing.
2018-06-21 | GSE116064 | GEO
Project description:We found PEAT complexes mediate histone deacetylation and heterochromatin condensation and thereby facilitate heterochromatin silencing.
2018-06-21 | GSE116067 | GEO
Project description:Occupancy profiling of Rec12 during fission yeast meiosis. Facultative heterochromatin regulates gene expression, but its assembly is poorly understood. Previously, we identified facultative heterochromatin islands in the fission yeast genome and found that RNA elimination machinery promotes island assembly at meiotic genes. Here, we report that Taz1, a component of the telomere protection complex Shelterin, is required to assemble heterochromatin islands at regions corresponding to late replication origins that are sites of double-strand break formation during meiosis. The loss of Taz1 and other Shelterin subunits, including Ccq1 that interacts with Clr4/Suv39h, abolishes heterochromatin at late origins and causes defective silencing of associated genes. Moreover, the late origin regulator Rif1 affects heterochromatin at Taz1-dependent islands and subtelomeric regions. We uncover a connection between heterochromatin and replication control, and show that heterochromatin factors affect timing of replication. These analyses implicate Shelterin in facultative heterochromatin assembly at late origins, which has important implications for the maintenance of genome stability and gene regulation. Whole cell extract DNA and DNA recovered by Rec12 ChIP from fission yeast undergoing synchronous meiosis were random-prime PCR amplified and labeled with Cy3 (whole cell extract) or Cy5 (IP DNA) and analyzed using custom 60mer Agilent array that tiles Schizosaccharomyces pombe genome in 300bp intervals alternately on both strands.
2016-06-09 | E-GEOD-78821 | biostudies-arrayexpress
Project description:Occupancy profiling of Shelterin components in fission yeast. Facultative heterochromatin regulates gene expression, but its assembly is poorly understood. Previously, we identified facultative heterochromatin islands in the fission yeast genome and found that RNA elimination machinery promotes island assembly at meiotic genes. Here, we report that Taz1, a component of the telomere protection complex Shelterin, is required to assemble heterochromatin islands at regions corresponding to late replication origins that are sites of double-strand break formation during meiosis. The loss of Taz1 and other Shelterin subunits, including Ccq1 that interacts with Clr4/Suv39h, abolishes heterochromatin at late origins and causes defective silencing of associated genes. Moreover, the late origin regulator Rif1 affects heterochromatin at Taz1-dependent islands and subtelomeric regions. We uncover a connection between heterochromatin and replication control, and show that heterochromatin factors affect timing of replication. These analyses implicate Shelterin in facultative heterochromatin assembly at late origins, which has important implications for the maintenance of genome stability and gene regulation. Whole cell extract DNA and DNA recovered from Taz1 or Rif1-immunoprecipitated chromatin of fission yeast were random-prime PCR amplified and labeled with Cy3 (whole cell extract DNA) or with Cy5 (IP DNA) and analyzed using custom 60mer Agilent array that tiles Schizosaccharomyces pombe genome in 300bp intervals alternately on both strands.
2016-06-09 | E-GEOD-78822 | biostudies-arrayexpress
Project description:ChIP-chip analyses of lysine 9 dimethylated histone H3 in Shelterin mutants. Facultative heterochromatin regulates gene expression, but its assembly is poorly understood. Previously, we identified facultative heterochromatin islands in the fission yeast genome and found that RNA elimination machinery promotes island assembly at meiotic genes. Here, we report that Taz1, a component of the telomere protection complex Shelterin, is required to assemble heterochromatin islands at regions corresponding to late replication origins that are sites of double-strand break formation during meiosis. The loss of Taz1 and other Shelterin subunits, including Ccq1 that interacts with Clr4/Suv39h, abolishes heterochromatin at late origins and causes defective silencing of associated genes. Moreover, the late origin regulator Rif1 affects heterochromatin at Taz1-dependent islands and subtelomeric regions. We uncover a connection between heterochromatin and replication control, and show that heterochromatin factors affect timing of replication. These analyses implicate Shelterin in facultative heterochromatin assembly at late origins, which has important implications for the maintenance of genome stability and gene regulation. Whole cell extract DNA and DNA recovered from H3K9 dimethylated chromatin of fission yeast were random-prime PCR amplified and labeled with Cy3 (whole cell extract) or Cy5 (IP DNA) and analyzed using custom 60mer Agilent array that tiles Schizosaccharomyces pombe genome in 300bp intervals alternately on both strands.
2016-06-09 | E-GEOD-78820 | biostudies-arrayexpress
Project description:BrdU profiling of replication activity in hydroxyurea treated synchronous culture of fission yeast. Facultative heterochromatin regulates gene expression, but its assembly is poorly understood. Previously, we identified facultative heterochromatin islands in the fission yeast genome and found that RNA elimination machinery promotes island assembly at meiotic genes. Here, we report that Taz1, a component of the telomere protection complex Shelterin, is required to assemble heterochromatin islands at regions corresponding to late replication origins that are sites of double-strand break formation during meiosis. The loss of Taz1 and other Shelterin subunits, including Ccq1 that interacts with Clr4/Suv39h, abolishes heterochromatin at late origins and causes defective silencing of associated genes. Moreover, the late origin regulator Rif1 affects heterochromatin at Taz1-dependent islands and subtelomeric regions. We uncover a connection between heterochromatin and replication control, and show that heterochromatin factors affect timing of replication. These analyses implicate Shelterin in facultative heterochromatin assembly at late origins, which has important implications for the maintenance of genome stability and gene regulation. Cdc25-22 cells carrying thymidine kinase and human nucleoside transporter expression modules were arrested at the G2/M boundary. After release into the cell cycle in minimal medium supplemented with hydroxyurea and 5â-bromo-2â-deoxyuridine (BrdU) cells were collected at time corresponding to maximal septation index and fixed by treatment with sodium azide. BrdU labeled DNA was recovered by immunoprecipitation, amplified by random-primed PCR and after conjugation with Cy5 (IP) or Cy3 (input DNA) analyzed on Agilent 60mer array.
2016-06-09 | E-GEOD-78819 | biostudies-arrayexpress