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The RPD3L deacetylation complex is required for facultative heterochromatin repression in Neurospora crassa [Mnase-seq]

ABSTRACT: The RPD3L deacetylation complex is required for facultative heterochromatin repression in Neurospora crassa [Mnase-seq]

PROVIDER: PRJNA1086494 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28291446_1.fastq.gz	Fastqsanger.gz
	SRR28291446_2.fastq.gz	Fastqsanger.gz
	SRR28291447_1.fastq.gz	Fastqsanger.gz
	SRR28291447_2.fastq.gz	Fastqsanger.gz
	SRR28291448_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

The RPD3L deacetylation complex is required for facultative heterochromatin repression in Neurospora crassa [Mnase-seq]

Project description:Repression of facultative heterochromatin is essential for developmental processes in numerous organisms. Methylation of histone H3 lysine 27 (H3K27) by Polycomb repressive complex 2 is a prominent feature of facultative heterochromatin in both fungi and higher eukaryotes. Although this methylation is frequently crucial for silencing, the detailed mechanism of repression remains poorly understood. We utilized a forward genetics approach to identify three previously uncharacterized genes required to maintain silencing at facultative heterochromatin genes in Neurospora crassa: sds3 (NCU01599), rlp1 (RPD3L protein 1; NCU09007) and rlp2 (RPD3L protein 2; NCU02898). We found that SDS3, RLP1, and RLP2 associate with N. crassa homologs of the Saccharomyces cerevisiae RPD3L complex and are required for repression of a subset of H3K27-methylated genes. Loss of these genes does not lead to loss of H3K27 methylation but increases acetylation of histone H3 lysine 14 at upregulated genes, and SDS3 binding levels are highest at genes derepressed upon loss of sds3, rlp1, and rlp2, implying that RPD3L-driven deacetylation is a previously undescribed factor required for silencing of facultative heterochromatin in N. crassa.

2024-08-21 | GSE261325 | GEO

The RPD3L deacetylation complex is required for facultative heterochromatin repression in Neurospora crassa [ChIP-seq]

2024-08-21 | GSE261327 | GEO

The RPD3L deacetylation complex is required for facultative heterochromatin repression in Neurospora crassa [RNA-seq]

2024-08-21 | GSE261319 | GEO

The RPD3L deacetylation complex is required for facultative heterochromatin repression in Neurospora crassa [RNA-seq]

Project description:The RPD3L deacetylation complex is required for facultative heterochromatin repression in Neurospora crassa [RNA-seq]

| PRJNA1086483 | ENA

The RPD3L deacetylation complex is required for facultative heterochromatin repression in Neurospora crassa [ChIP-seq]

Project description:The RPD3L deacetylation complex is required for facultative heterochromatin repression in Neurospora crassa [ChIP-seq]

| PRJNA1086495 | ENA

Histone deacetylation promotes transcriptional silencing at facultative heterochromatin

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

Histone deacetylation promotes transcriptional silencing at facultative heterochromatin

Project description:Histone deacetylation promotes transcriptional silencing at facultative heterochromatin

| PRJNA428233 | ENA

Rpd3L HDAC links H3K4me3 to transcriptional repression memory

Project description:Transcriptional memory is critical for the faster reactivation of necessary genes upon environmental changes and requires that the genes were previously in an active state. However, whether transcriptional repression also displays “memory” of the prior transcriptionally inactive state remains unknown. In this study, we show that transcriptional repression of approximately 540 genes in yeast occurs much more rapidly if the genes have been previously repressed during carbon source shifts. This novel transcriptional response has been termed transcriptional repression memory(TREM). Interestingly, Rpd3L histone deacetylase (HDAC), targeted to active promoters induces TREM. Mutants for Rpd3L exhibit increased acetylation at active promoters and delay TREM and RNA PolII dissociation significantly. Surprisingly, the interaction between H3K4me3 and Rpd3L via the Pho23 PHD finger is sufficient to induce histone deacetylation and TREM by Rpd3L. Therefore, we propose that an active mark, H3K4me3 enriched at promoters, instructs Rpd3L HDAC to induce histone deacetylation and TREM.

2018-10-23 | E-MTAB-6551 | biostudies-arrayexpress

Taz1-Shelterin promotes facultative heterochromatin assembly at chromosome-internal sites containing late replication origins [Rec12]

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

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.

2016-06-09 | E-GEOD-78822 | biostudies-arrayexpress

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