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CHD1 in yeast is recruited by transcription elongation factors and maintains H3K4me3/H3K36me3 domains at actively transcribed and spliced genes

ABSTRACT: CHD1 in yeast is recruited by transcription elongation factors and maintains H3K4me3/H3K36me3 domains at actively transcribed and spliced genes

PROVIDER: PRJNA356615 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5085170_1.fastq.gz	Fastqsanger.gz
	SRR5085170_2.fastq.gz	Fastqsanger.gz
	SRR5085180_1.fastq.gz	Fastqsanger.gz
	SRR5085180_2.fastq.gz	Fastqsanger.gz
	SRR5085190_1.fastq.gz	Fastqsanger.gz

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CHD1 in yeast is recruited by transcription elongation factors and maintains H3K4me3/H3K36me3 domains at actively transcribed and spliced genes

Project description:Chd1 is a conserved ATP-dependent chromatin remodeler that maintains the nucleosomal structure of chromatin, but the determinants of its specificity and its impact on gene expression are not well defined. To identify the determinants of Chd1 binding specificity in the yeast genome, we investigated Chd1 occupancy in mutants of several candidate factors. We found that several components of the PAF1 transcription elongation complex contribute to Chd1 recruitment to highly transcribed genes, and identified Spt4 as a factor that appears to negatively modulate Chd1 binding to chromatin. We discovered that CHD1 loss alters H3K4me3 and H3K36me3 patterns throughout the yeast genome. Interestingly, the aberrant histone H3 methylation patterns were predominantly observed within 1 kb from the transcription start site, where both histone H3 methylation marks co-occur. A reciprocal change between the two marks was obvious in the absence of Chd1, suggesting a role for CHD1 in establishing or maintaining the boundaries of these largely mutually exclusive histone marks. Strikingly, intron-containing genes were most susceptible to CHD1 loss, and exhibited a high degree of histone H3 methylation changes. Intron retention was significantly lower in the absence of CHD1, suggesting that CHD1 function as a chromatin remodeler could indirectly affect RNA splicing. This SuperSeries is composed of the SubSeries listed below.

2017-04-26 | GSE90998 | GEO

CHD1 in yeast is recruited by transcription elongation factors and maintains H3K4me3/H3K36me3 domains at actively transcribed and spliced genes [ChIP-seq]

Project description:We report genome-wide Chd1 occupancy in WT and in ten elongation factor mutants, and genome-wide H3K4me3/H3K36me3 profiles in WT and CHD1 mutant.

2017-04-26 | GSE90996 | GEO

CHD1 in yeast is recruited by transcription elongation factors and maintains H3K4me3/H3K36me3 domains at actively transcribed and spliced genes [RNA-seq]

Project description:We report quantitative transcriptome data in WT and CHD1 mutant.

2017-04-26 | GSE90997 | GEO

The ATP-dependent chromatin remodeler Chd1 is recruited by transcription elongation factors and maintains H3K4me3/H3K36me3 domains at actively transcribed and spliced genes.

Project description:Chd1 (Chromodomain Helicase DNA Binding Protein 1) is a conserved ATP-dependent chromatin remodeler that maintains the nucleosomal structure of chromatin, but the determinants of its specificity and its impact on gene expression are not well defined. To identify the determinants of Chd1 binding specificity in the yeast genome, we investigated Chd1 occupancy in mutants of several candidate factors. We found that several components of the PAF1 transcription elongation complex contribute to Chd1 recruitment to highly transcribed genes and identified Spt4 as a factor that appears to negatively modulate Chd1 binding to chromatin. We discovered that CHD1 loss alters H3K4me3 and H3K36me3 patterns throughout the yeast genome. Interestingly, the aberrant histone H3 methylation patterns were predominantly observed within 1 kb from the transcription start site, where both histone H3 methylation marks co-occur. A reciprocal change between the two marks was obvious in the absence of Chd1, suggesting a role for CHD1 in establishing or maintaining the boundaries of these largely mutually exclusive histone marks. Strikingly, intron-containing genes were most susceptible to CHD1 loss and exhibited a high degree of histone H3 methylation changes. Intron retention was significantly lower in the absence of CHD1, suggesting that CHD1 function as a chromatin remodeler could indirectly affect RNA splicing.

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H3K36me3-mediated mismatch repair preferentially protects actively transcribed genes from mutation.

Project description:Histone H3 trimethylation at lysine 36 (H3K36me3) is an important histone mark involved in both transcription elongation and DNA mismatch repair (MMR). It is known that H3K36me3 recruits the mismatch-recognition protein MutS? to replicating chromatin via its physical interaction with MutS?'s PWWP domain, but the exact role of H3K36me3 in transcription is undefined. Using ChIP combined with whole-genome DNA sequencing analysis, we demonstrate here that H3K36me3, together with MutS?, is involved in protecting against mutation, preferentially in actively transcribed genomic regions. We found that H3K36me3 and MutS? are much more co-enriched in exons and actively transcribed regions than in introns and nontranscribed regions. The H3K36me3-MutS? co-enrichment correlated with a much lower mutation frequency in exons and actively transcribed regions than in introns and nontranscribed regions. Correspondingly, depleting H3K36me3 or disrupting the H3K36me3-MutS? interaction elevated the spontaneous mutation frequency in actively transcribed genes, but it had little influence on the mutation frequency in nontranscribed or transcriptionally inactive regions. Similarly, H2O2-induced mutations, which mainly cause base oxidations, preferentially occurred in actively transcribed genes in MMR-deficient cells. The data presented here suggest that H3K36me3-mediated MMR preferentially safeguards actively transcribed genes not only during replication by efficiently correcting mispairs in early replicating chromatin but also during transcription by directly or indirectly removing DNA lesions associated with a persistently open chromatin structure.

| S-EPMC5961058 | biostudies-literature

FACT is recruited to the +1 nucleosome of transcribed genes and spreads in a Chd1-dependent manner

Project description:FACT is recruited to the +1 nucleosome of transcribed genes and spreads in a Chd1-dependent manner

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Chemical modifications mark alternatively spliced and actively degrading messenger RNAs in Arabidopsis and humans

Project description:Chemical modifications mark alternatively spliced and actively degrading messenger RNAs in Arabidopsis and humans

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FACT is recruited to the +1 nucleosome of transcribed genes and spreads in a Chd1-dependent manner [ChIP-chip]

Project description:The histone chaperone FACT occupies transcribed regions where it plays prominent roles in maintaining chromatin integrity and preserving epigenetic information. How it is targeted to transcribed regions, however, remains unclear. Proposed models for how FACT finds its way to transcriptionally active chromatin include docking on the RNA polymerase II (RNAPII) C-terminal domain (CTD), recruitment by elongation factors, recognition of modified histone tails and binding partially disassembled nucleosomes. Here, we systematically tested these and other scenarios in Saccharomyces cerevisiae and found that FACT binds transcribed chromatin, not RNAPII. Through a combination of experimental and mathematical modeling evidence, we propose that FACT recognizes the +1 nucleosome, as it is partially unwrapped by the engaging RNAPII, and spreads to downstream nucleosomes aided by the chromatin remodeler Chd1. Our work clarifies how FACT interacts with genes, suggests a processive mechanism for FACT function, and provides a framework to further dissect the molecular mechanisms of transcription-coupled histone chaperoning.

2021-07-26 | GSE155110 | GEO

FACT is recruited to the +1 nucleosome of transcribed genes and spreads in a Chd1-dependent manner [ChIP-exo]

2021-07-26 | GSE155138 | GEO

FACT is recruited to the +1 nucleosome of transcribed genes and spreads in a Chd1-dependent manner [ChIP-chip]

Project description:FACT is recruited to the +1 nucleosome of transcribed genes and spreads in a Chd1-dependent manner [ChIP-chip]

| PRJNA648828 | ENA