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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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE182068 | GEO | 2022/01/01

REPOSITORIES: GEO

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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 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

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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.

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

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RNA -sequencing of high grade glioma (HGG) mouse cells encoding for H3.3-G34R vs H3.3-WT histones, derived from a Sleeping beauty based-genetically engineered mouse model

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 in a pediatric high grade glioma model, using a Sleeping beauty derived genetically engenieered mouse model.

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ChIP-sequencing of high grade glioma (HGG) mouse cells encoding for H3.3-G34R vs H3.3-WT histones, derived from a Sleeping beauty based-genetically engineered mouse model.

Project description:ChIP-sequencing of H3.3-G34R and H3.3-WT HGG cells was performed for several histone marks to uncover differences on histone mark deposition related to the presence of H3.3-G34R mutation, using a Sleeping beauty derived genetically engenieered mouse model.

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Differential gene expression in a mouse model for pediatric high grade glioma encoding for H3.3-G34R mutation

Project description:This experiment was designed to study the effect of the histone H3.3-G34R mutation on the transcriptome of tumor cells and immune-infiltrating cells, in a high grade glioma mouse model.

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Paediatric Glioma Histone H3.3 K27M/G34R Mutations Drive Abnormalities in Phase-Separated PML Nuclear Bodies.

Project description:Point mutations in histone variant H3.3 (H3.3 K27M, H3.3 G34R) and the H3.3-specific ATRX/DAXX chaperone complex are frequent events in paediatric gliomas. It is clear that H3.3 point mutations affect many chromatin modifications but the exact oncogenic mechanisms are an area of active investigation. Histone H3.3 has been previously linked to PML, a gene which is frequently mutated in Acute Promyelocytic Leukaemia. We find that H3.3 point mutations disrupt the formation of PML nuclear bodies and this prevents differentiation down glial lineages. Similar to PML-mutated Acute Promyelocytic Leukaemias, H3.3-mutated patient-derived gliomas cells are also sensitive to drugs which target PML bodies. We identify PML as a contributor to oncogenesis in H3.3-mutated gliomas and our results indicate that PML-targeting strategies may prove effective at treating H3.3-mutated paediatric gliomas.

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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

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

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

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Regional identity of human neural stem cells determines oncogenic responses to histone H3.3 mutants [ChIP-Seq]

Project description:Point mutations within the histone H3.3 are frequent in aggressive childhood brain tumours known as paediatric high-grade gliomas (pHGGs). Intriguingly, different mutations arise in discrete anatomical regions: H3.3-G34R within the forebrain and H3.3-K27M preferentially within the hindbrain. The reasons for this contrasting aetiology are unknown. By engineering human foetal neural stem cell cultures from distinct regions, we demonstrate here that cell-intrinsic regional identity provides differential responsiveness to each mutant that mirrors the origins of pHGGs. Focusing on H3.3-G34R, we find that the oncohistone supports proliferation of forebrain cells, while inducing a cytostatic response in the hindbrain. Mechanistically, H3.3-G34R does not impose widespread transcriptional or epigenetic changes, but impairs recruitment of ZMYND11, a transcriptional repressor of highly expressed genes. We therefore propose that H3.3-G34R promotes tumorigenesis by stabilising the expression of key progenitor genes and, thus, locking initiating forebrain cells into their preexisting immature state.

2021-03-24 | GSE163185 | GEO

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