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A conserved factor Dhp1/Rat1/Xrn2 triggers premature transcription termination and nucleates heterochromatin to promote gene silencing [ChIP-chip]

ABSTRACT: Occupancy profiling of lysine 9 dimethylated histone H3 in fission yeast. Occupancy profiling of Red1, Mtl1, and Mmi1 proteins in fission yeast. Agilent 60mer array was used to analyze DNA recovered by immunoprecipitation of lysine 9 dimethylated histone H3, Red1, Mtl1, and Mmi1 proteins from asynchronous culture of fission yeast.

ORGANISM(S): Schizosaccharomyces pombe

SUBMITTER: Shiv Grewal

PROVIDER: E-GEOD-74740 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Conserved factor Dhp1/Rat1/Xrn2 triggers premature transcription termination and nucleates heterochromatin to promote gene silencing.

Chalamcharla Venkata R VR Folco H Diego HD Dhakshnamoorthy Jothy J Grewal Shiv I S SI

Proceedings of the National Academy of Sciences of the United States of America 20151202 51

Cotranscriptional RNA processing and surveillance factors mediate heterochromatin formation in diverse eukaryotes. In fission yeast, RNAi machinery and RNA elimination factors including the Mtl1-Red1 core and the exosome are involved in facultative heterochromatin assembly; however, the exact mechanisms remain unclear. Here we show that RNA elimination factors cooperate with the conserved exoribonuclease Dhp1/Rat1/Xrn2, which couples pre-mRNA 3'-end processing to transcription termination, to pr ...[more]

PMID: 26631744

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A conserved factor Dhp1/Rat1/Xrn2 triggers premature transcription termination and nucleates heterochromatin to promote gene silencing [ChIP-chip]

Project description:Occupancy profiling of lysine 9 dimethylated histone H3 in fission yeast. Occupancy profiling of Red1, Mtl1, and Mmi1 proteins in fission yeast.

2016-01-05 | GSE74740 | GEO

Taz1-Shelterin promotes facultative heterochromatin assembly at chromosome-internal sites containing late replication origins [H3K9me2]

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

Taz1-Shelterin promotes facultative heterochromatin assembly at chromosome-internal sites containing late replication origins [Taz1]

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.

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A conserved factor Dhp1/Rat1/Xrn2 triggers premature transcription termination and nucleates heterochromatin to promote gene silencing

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Taz1-Shelterin promotes facultative heterochromatin assembly at chromosome-internal sites containing late replication origins

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