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Rpd3L Contributes to the DNA Damage Sensitivity of Saccharomyces cerevisiae Checkpoint Mutants

ABSTRACT: Rpd3L Contributes to the DNA Damage Sensitivity of Saccharomyces cerevisiae Checkpoint Mutants

PROVIDER: PRJNA454307 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7084540_1.fastq.gz	Fastqsanger.gz
	SRR7084540_2.fastq.gz	Fastqsanger.gz
	SRR7084550_1.fastq.gz	Fastqsanger.gz
	SRR7084550_2.fastq.gz	Fastqsanger.gz
	SRR7084560_1.fastq.gz	Fastqsanger.gz

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Rpd3L Contributes to the DNA Damage Sensitivity of Saccharomyces cerevisiae Checkpoint Mutants

Project description:DNA replication forks that are stalled by DNA damage activate an S phase checkpoint that prevents irreversible fork arrest and cell death. The increased cell death caused by DNA damage in budding yeast cells lacking the Rad53 checkpoint protein kinase is partially suppressed by deletion of the EXO1 gene. Here,we identified that loss of the histone deacetylase complex Rpd3L promotes survival of rad53∆ cells exposed to DNA damaging agents. From epistasis analysis, we show that this suppression operates in a separate pathway from the previously described suppression by deletion of EXO1.

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Rpd3L Contributes to the DNA Damage Sensitivity of Saccharomyces cerevisiae Checkpoint Mutants.

Project description:DNA replication forks that are stalled by DNA damage activate an S-phase checkpoint that prevents irreversible fork arrest and cell death. The increased cell death caused by DNA damage in budding yeast cells lacking the Rad53 checkpoint protein kinase is partially suppressed by deletion of the EXO1 gene. Using a whole-genome sequencing approach, we identified two additional genes, RXT2 and RPH1, whose mutation can also partially suppress this DNA damage sensitivity. We provide evidence that RXT2 and RPH1 act in a common pathway, which is distinct from the EXO1 pathway. Analysis of additional mutants indicates that suppression works through the loss of the Rpd3L histone deacetylase complex. Our results suggest that the loss or absence of histone acetylation, perhaps at stalled forks, may contribute to cell death in the absence of a functional checkpoint.

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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.

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

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

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Rpd3L HDAC links H3K4me3 to transcriptional repression memory

Project description:Rpd3L HDAC links H3K4me3 to transcriptional repression memory

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