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

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

ORGANISM(S): Saccharomyces cerevisiae

PROVIDER: GSE90997 | GEO | 2017/04/26

SECONDARY ACCESSION(S): PRJNA356619

REPOSITORIES: GEO

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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

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.

| S-EPMC5499586 | biostudies-literature

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

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

| PRJNA356615 | ENA

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 MutSα to replicating chromatin via its physical interaction with MutSα'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 MutSα, is involved in protecting against mutation, preferentially in actively transcribed genomic regions. We found that H3K36me3 and MutSα are much more co-enriched in exons and actively transcribed regions than in introns and nontranscribed regions. The H3K36me3-MutSα 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-MutSα 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

Chd1 co-occupancy with early transcription elongation factors

Project description:We report the genome-wide Chd1 co-occupancy with early transcription elongation factors ChIP-seq for Chd1 and elongating RNA polymerase II

2014-10-23 | E-GEOD-56061 | biostudies-arrayexpress

A Key Role for Chd1 in Histone H3 Dynamics at the 3' Ends of Long Genes in Yeast (H3K4me3 or H3K36me3 to input)

Project description:Chd proteins are ATP-dependent chromatin remodeling enzymes implicated in biological functions from transcriptional elongation to control of pluripotency. Here, we examine roles of Chd1 in replication- independent dynamics of histone H3 in yeast. Using genome-wide ChIP on chip analysis, we find that Chd1 influences histone turnover at the 5’ and 3’ ends of genes, accelerating H3 replacement at the 5’ ends of genes while protecting the 3’ ends of genes from excessive H3 turnover. Although consistent with a direct role for Chd1 in exchange, these results may indicate that Chd1 stabilizes nucleosomes perturbed by transcription. Curiously, we observe a strong effect of gene length on Chd1’s effects on H3 turnover. Finally, we show that Chd1 also affects histone H3K4 and H3K36 methylation patterns over genes, likely as a consequence of its effects on histone replacement. In control experiments, we measure effects of deletion of CHD1 on RNA polymerase II distribution across the genome and on gene expression. We also examine the effect of deleting the TOP1 gene, alone and in combination with deletion of CHD1, on histone replacement. Taken together, our results emphasize a role for Chd1 in histone replacement in both budding yeast and Drosophila, and surprisingly show that the major effects of Chd1 on turnover occur at the 3’ ends of genes.

2012-06-08 | GSE38492 | GEO

A Key Role for Chd1 in Histone H3 Dynamics at the 3' Ends of Long Genes in Yeast (H3K4me3 or H3K36me3 to input)

Project description:Chd proteins are ATP-dependent chromatin remodeling enzymes implicated in biological functions from transcriptional elongation to control of pluripotency. Here, we examine roles of Chd1 in replication- independent dynamics of histone H3 in yeast. Using genome-wide ChIP on chip analysis, we find that Chd1 influences histone turnover at the 5M-bM-^@M-^Y and 3M-bM-^@M-^Y ends of genes, accelerating H3 replacement at the 5M-bM-^@M-^Y ends of genes while protecting the 3M-bM-^@M-^Y ends of genes from excessive H3 turnover. Although consistent with a direct role for Chd1 in exchange, these results may indicate that Chd1 stabilizes nucleosomes perturbed by transcription. Curiously, we observe a strong effect of gene length on Chd1M-bM-^@M-^Ys effects on H3 turnover. Finally, we show that Chd1 also affects histone H3K4 and H3K36 methylation patterns over genes, likely as a consequence of its effects on histone replacement. In control experiments, we measure effects of deletion of CHD1 on RNA polymerase II distribution across the genome and on gene expression. We also examine the effect of deleting the TOP1 gene, alone and in combination with deletion of CHD1, on histone replacement. Taken together, our results emphasize a role for Chd1 in histone replacement in both budding yeast and Drosophila, and surprisingly show that the major effects of Chd1 on turnover occur at the 3M-bM-^@M-^Y ends of genes. ChIP on chip experiments, comparing IP to input.

2012-06-07 | E-GEOD-38492 | biostudies-arrayexpress

Chd1 co-occupancy with early transcription elongation factors

Project description:We report the genome-wide Chd1 co-occupancy with early transcription elongation factors

2014-10-23 | GSE56061 | GEO

CHD1 and H3K4me3 ChIP-seq in prostate cancer cell line PC-3

Project description:Trimethylation of histone H3 at lysine 4 (H3K4me3) is known to be associated with transcriptional activation and CHD1 is known to selectively recognize and bind to H3K4me3 to activate gene transcription. In addition, CHD1 is involved in the maintenance of open chromatin and cooperates with H3K4me3 to control pluripotency of murine embryonic stem cells. To determine the downstream transcriptional targets and pathways of CHD1 and H3K4me3 in PTEN-null PCa cells, ChIP-seq was performed in control versus CHD1 knockdown PC-3 cells.

2017-02-10 | GSE91401 | GEO

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