Rpd3L HDAC links H3K4me3 to transcriptional repression memory
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB25263 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR2356730_1.fastq.gz | Fastqsanger.gz | |||
| ERR2356730_2.fastq.gz | Fastqsanger.gz | |||
| ERR2356740_1.fastq.gz | Fastqsanger.gz | |||
| ERR2356740_2.fastq.gz | Fastqsanger.gz | |||
| ERR2356731_1.fastq.gz | Fastqsanger.gz |
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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
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 ∼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 significantly. Surprisingly, the interaction between H3K4me3 and Rpd3L via the Pho23 PHD finger is critical to promote histone deacetylation and TREM by Rpd3L. Therefore, we propose that an active mark, H3K4me3 enriched at active promoters, instructs Rpd3L HDAC to induce histone deacetylation and TREM.
| S-EPMC6144869 | biostudies-literature
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 | GSE261327 | GEO
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
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 | GSE261319 | GEO
Project description:In yeast, NuA3 histone acetyltransferase (NuA3 HAT) enhances H3K14 acetylation and transcription of a subset gene via interaction between the Yng1 PHD finger and H3K4me3. Although NuA3 HAT includes multiple chromatin binding modules with distinct specificities, their interdependencies and combinatorial actions in chromatin binding and transcription remain unknown. Modified peptide pulldown assays reveal that Yng1 n-terminal region is important for the integrity of NuA3 HAT by mediating interaction between core subunits and two methyl-binders, Yng1and Pdp3. We further uncover that NuA3 HAT contributes to both Rpd3S and Rpd3L HDACs-mediated regulation of mRNA and lncRNA expression dynamics. Yng1 n-terminal region, Nto1 PHD finger and Pdp3 PWWP domain are important for optimal induction of mRNA and cryptic transcription repressed by the Set2-Rpd3S HDAC pathway. In contrast, the Yng1 PHD finger-H3K4me3 interaction affects transcriptional repression memory (TREM) regulated by Rpd3L HDAC. These findings suggest that NuA3 HAT utilizes distinct chromatin readers to compete with two Rpd3 containing HDACs for optimal mRNA and lncRNA expression dynamics.
2020-09-08 | GSE148674 | GEO
Project description:Tissue fibrosis is a chronic disease driven by persistent fibroblast activation that has recently been linked to epigenetic modifications. Here, we screened a small library of epigenetic small-molecule modulators to identify compounds capable of inhibiting or reversing TGFβ-mediated fibroblast activation. We identified pracinostat, an HDAC inhibitor, as a potent attenuator of lung fibroblast activation and confirmed its efficacy in patient-derived fibroblasts isolated from fibrotic lung tissue. Mechanistically, we found that HDAC-dependent transcriptional repression was an early and essential event in TGFβ-mediated fibroblast activation. Treatment of lung fibroblasts with pracinostat broadly attenuated TGFβ-mediated epigenetic repression and promoted fibroblast quiescence. We confirmed a specific role for HDAC-dependent histone deacetylation in the promoter region of the anti-fibrotic gene PPARGC1A (PGC1α) in response to TGFβ stimulation. Finally, we identified HDAC7 as a key factor whose RNAi-mediated knockdown attenuates fibroblast activation without altering global histone acetylation. Together these results provide novel mechanistic insight into the essential role HDACs play in TGFβ-mediated fibroblast activation via targeted gene repression.
2019-08-29 | GSE136534 | GEO
Project description:The RPD3L deacetylation complex is required for facultative heterochromatin repression in Neurospora crassa [RNA-seq]
| PRJNA1086483 | ENA
Project description:The RPD3L deacetylation complex is required for facultative heterochromatin repression in Neurospora crassa [ChIP-seq]
| PRJNA1086495 | ENA
Project description:The RPD3L deacetylation complex is required for facultative heterochromatin repression in Neurospora crassa [Mnase-seq]
| PRJNA1086494 | ENA