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Histone H3-G34V and H3-G34R mutant fission yeast exhibit distinct chromatin changes and different DNA damage sensitivities.

ABSTRACT: Histone H3-G34V and H3-G34R mutant fission yeast exhibit distinct chromatin changes and different DNA damage sensitivities.

PROVIDER: PRJNA418713 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6297440_1.fastq.gz	Fastqsanger.gz
	SRR6297440_2.fastq.gz	Fastqsanger.gz
	SRR6297441_1.fastq.gz	Fastqsanger.gz
	SRR6297441_2.fastq.gz	Fastqsanger.gz
	SRR6297442_1.fastq.gz	Fastqsanger.gz

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Histone H3-G34V and H3-G34R mutant fission yeast exhibit distinct chromatin changes and different DNA damage sensitivities.

Project description:Recurrent somatic mutations of H3F3A in aggressive pediatric high-grade gliomas generate K27M or G34R mutant histone H3.3. H3.3-G34R mutants are common in tumors additionally mutant for p53 and ATRX, an H3.3-specific chromatin remodeler. To gain insight into the role of H3-G34R, we generated fission yeast that express only the mutant histone H3. H3-G34R specifically reduces H3K36 tri-methylation and H3K36 acetylation, but minimally affects transcriptional control. H3-G34R mutants exhibit genomic instability and increased replicative stress including slowed replication fork restart although DNA replication checkpoints are functional. H3-G34R mutants are defective for DNA damage repair by homologous recombination (HR), and on damage have altered HR protein dynamics suggestive that H3-G34R slows resolution of HR-mediated repair. In summary our analysis of H3-G34R mutant fission yeast provides mechanistic insight into how G34R mutation may promote genomic instability in glioma.

2018-11-15 | GSE106979 | GEO

Histone H3G34R mutation causes replicative stress, defective homologous recombination and genomic instability in Fission Yeast

2017-07-20 | GSE96842 | GEO

Surprising Phenotypic Diversity of Cancer-associated mutations at Gly 34 in the Histone H3 tail

Project description:Deep sequencing of cancer genomes has identified frequent mutation of core histones, termed oncohistones, but the role of some mutants is poorly understood. Here, using fission yeast as a model, we determine the consequences of mutation of histone H3.3 at Gly 34, a site frequently mutated in pediatric cortical high-grade glioma (G34R/V), and in virtually all giant cell tumors of bone (G34W). H3-G34 mutations cause a surprising diversity of outcomes, differentially affecting modification of the nearby H3K36 residue, subtelomeric silencing, genomic stability, sensitivity to irradiation, alkylating agents, hydroxyurea and influencing DNA repair. Since fifteen genes encode H3 isoforms, and only one allele is targeted in cancer, G34R/V/W H3 likely represents a small portion of total cellular H3. Whilst the presence of wild type H3 rescues most G34 mutant phenotypes, hydroxyurea sensitivity, subtelomeric silencing and homologous recombination defects dominate in cells expressing G34R and wild type H3. Together, these studies demonstrate the complexity associated with different substitutions at even a single residue in histone H3 and highlight the utility of genetically tractable systems for their analysis.

2021-02-08 | GSE162572 | GEO

RNA-seq in WT and H3.3 G34R mouse ES cells

Project description:Sequencing of paediatric gliomas has identified two common substitution mutations (K27M and G34R) in genes encoding histone H3.3. We introduced a single-copy H3.3 G34R targeted mutation in mouse ES cells and observed gains in H3K36me3 and H3K9me3 across the genome. Altered chromatin profiles correlated with enrichment of KDM4 A/B/C, a histone lysine (K9/K36) demethylase. RNA-seq of H3.3 G34R mutant showed disrupted gene expression patterns which also correlated with KDM4 enrichment. Expression of a single copy of H3.3 G34R at endogenous levels was sufficient to genocopy KDM4 triple-KO cells as determined by ChIP-seq and RNA-seq.

2018-07-08 | GSE106204 | GEO

ChIP-seq of histone H3 and H3K9me2 in WT and dbl2 mutant fission yeast

Project description:The aim was to compare the levels of histone H3 dimethylation at lysine 9 (H3K9me2) in wild-type and dbl2 knock-out Schizosaccharomyces pombe cells. Fission yeast cultures were grown in the complex YES medium to exponential phase and chromatin immunoprecipitation was carried out using anti-H3 and anti-H3K9me2 antibodies. Two independent biological replicates were performed. The resulting IP and input DNA samples were sequenced using Illumina sequencing (35 nt PE). H3K9me2 occupancy in each sample was normalized to the corresponding total H3 occupancy, and normalized H3K9me2 levels were compared between WT and dbl2 knock-out.

2020-10-02 | E-MTAB-9619 | biostudies-arrayexpress

H3K9me3 and H3K36me3 ChIP-seq in WT and H3.3 G34R mouse ES cells

2018-07-08 | GSE106203 | GEO

Cohesin has a deleterious effect on heterochromatin assembly in fission yeast cells lacking Pds5

Project description:Occupancy profiling of lysine 9 dimethylated histone H3 in fission yeast. Occupancy profiling of Pds5 proteins in fission yeast.

2020-04-22 | GSE130233 | GEO

Histone H3 lysine9 acetylation, rather than lysine4 trimethylation, marks meiotic recombination hotspots and promotes recombination initiation in fission yeast

Project description:Histone modifications are associated with meiotic recombination hotspots, discrete sites with augmented recombination frequency. For example, trimethylation of histone H3 lysine4 (H3K4me3) marks most hotspots in budding yeast and mouse. Modified histones are known to regulate meiotic recombination partly by promoting DNA double strand break (DSB) formation, but the role and precise landscape of histone modifications at hotspots remain unclear. Here, we studied hotspot-associated modifications in fission yeast and found general features: acetylation of H3 lysine9 (H3K9ac) is strikingly elevated, and H3K4me3 is not significantly enriched. Remarkably, elimination of H3K9ac reduced binding of the DSB-inducing enzyme Rec12 and DSB at hotspots. We also found that the H3K4 metyltransferase Set1 promotes DSB formation at some loci, but it restricts Rec12 binding to hotspots. These results suggest that H3K9ac rather than H3K4me3 is a hotspot-associated mark involved in meiotic DSB formation in fission yeast.

2013-03-07 | GSE31648 | GEO

Factors that promote H3 chromatin integrity during transcription prevent promiscuous deposition of CENP-A(Cnp1) in fission yeast

Project description:Specialized chromatin containing CENP-A nucleosomes instead of H3 nucleosomes is found at all centromeres. However, the mechanisms that specify the locations at which CENP-A chromatin is assembled remain elusive in organisms with regional, epigenetically regulated centromeres. It is known that normal centromeric DNA is transcribed in several systems including the fission yeast, Schizosaccharomyces pombe. Here, we show that factors which preserve stable histone H3 chromatin during transcription also play a role in preventing promiscuous CENP-A(Cnp1) deposition in fission yeast. Mutations in the histone chaperone FACT impair the maintenance of H3 chromatin on transcribed regions and promote widespread CENP-A(Cnp1) incorporation at non-centromeric sites. FACT has little or no effect on CENP-A(Cnp1) assembly at endogenous centromeres where CENP-A(Cnp1) is normally assembled. In contrast, Clr6 complex II (Clr6-CII; equivalent to Rpd3S) histone deacetylase function has a more subtle impact on the stability of transcribed H3 chromatin and acts to prevent the ectopic accumulation of CENP-A(Cnp1) at specific loci, including subtelomeric regions, where CENP-A(Cnp1) is preferentially assembled. Moreover, defective Clr6-CII function allows the de novo assembly of CENP-A(Cnp1) chromatin on centromeric DNA, bypassing the normal requirement for heterochromatin. Thus, our analyses show that alterations in the process of chromatin assembly during transcription can destabilize H3 nucleosomes and thereby allow CENP-A(Cnp1) to assemble in its place. We propose that normal centromeres provide a specific chromatin context that limits reassembly of H3 chromatin during transcription and thereby promotes the establishment of CENP-A(Cnp1) chromatin and associated kinetochores. These findings have important implications for genetic and epigenetic processes involved in centromere specification.

2015-02-19 | GSE66106 | GEO

RNA-sequencing of high grade glioma (HGG) human cells encoding for H3.3-G34R vs H3.3-WT histones, derived from a patient harboring pHGG and stably tranfected with 3X-FLAG-tagged wild type H3.3 or a 3X-FLAG-tagged H3.3 harboring the G34R mutation

Project description:RNA-sequencing of H3.3-G34R and H3.3-WT HGG cells was performed to uncover transcriptomic differences related to the presence of H3.3-G34R mutation, using human cells obtained from a patient harboring pHGG and stably tranfected with 3X-FLAG-tagged wild type H3.3 or a 3X-FLAG-tagged H3.3 harboring the G34R mutation.

2022-01-01 | GSE182068 | GEO

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