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Disruption of H3K36 methylation provokes cellular plasticity to drive aberrant glandular formation and squamous carcinogenesis (Spatial Transcriptomics)

ABSTRACT: To investigate the role H3K36 methylation in stratifying epithelia

ORGANISM(S): Mus musculus

PROVIDER: GSE247994 | GEO | 2023/12/01

REPOSITORIES: GEO

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Disruption of H3K36 methylation provokes cellular plasticity to drive aberrant glandular formation and squamous carcinogenesis (RNA-Seq)

Project description:To investigate the role H3K36 methylation in stratifying epithelia

2023-12-01 | GSE247992 | GEO

Disruption of H3K36 methylation provokes cellular plasticity to drive aberrant glandular formation and squamous carcinogenesis (CUT&RUN)

Project description:To investigate the role H3K36 methylation in stratifying epithelia

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Disruption of H3K36 methylation provokes cellular plasticity to drive aberrant glandular formation and squamous carcinogenesis

Project description:This SuperSeries is composed of the SubSeries listed below.

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Disruption of H3K36 methylation provokes cellular plasticity to drive aberrant glandular formation and squamous carcinogenesis

Project description:Disruption of H3K36 methylation provokes cellular plasticity to drive aberrant glandular formation and squamous carcinogenesis

| PRJNA1041369 | ENA

Disruption of H3K36 methylation provokes cellular plasticity to drive aberrant glandular formation and squamous carcinogenesis (Spatial Transcriptomics)

Project description:Disruption of H3K36 methylation provokes cellular plasticity to drive aberrant glandular formation and squamous carcinogenesis (Spatial Transcriptomics)

| PRJNA1041374 | ENA

Disruption of H3K36 methylation provokes cellular plasticity to drive aberrant glandular formation and squamous carcinogenesis (CUT&RUN)

Project description:Disruption of H3K36 methylation provokes cellular plasticity to drive aberrant glandular formation and squamous carcinogenesis (CUT&RUN)

| PRJNA1041376 | ENA

Disruption of H3K36 methylation provokes cellular plasticity to drive aberrant glandular formation and squamous carcinogenesis (RNA-Seq)

Project description:Disruption of H3K36 methylation provokes cellular plasticity to drive aberrant glandular formation and squamous carcinogenesis (RNA-Seq)

| PRJNA1041375 | ENA

Histone H3.3 G34 mutations promote aberrant PRC2 activity and drive tumor progression [RNA-Seq]

Project description:A remarkably high frequency of pediatric gliomas and bone tumors harbor monoallelic, missense mutations in genes encoding histone variant H3.3 at Glycine 34. We find that G34 mutations distinctly impede H3K36 methylation by SETD2. Consequently, the reduction of H3K36 methylation leads to high levels of PRC2-mediated H3K27me3 on G34 mutant nucleosomes. We find that H3.3G34W expression in murine mesenchymal stem cells (mMSCs) promotes aberrant gain of H3K27me2/3 and loss of H3K27ac at active enhancers containing SETD2. mMSCs expressing H3.3G34W display a unique transcriptional program that is dependent on PRC2 activity *in cis* and exhibit enhanced tumor development *in vivo*. Altogether, we demonstrate that H3.3G34 oncohistones selectively promote PRC2 activity by interfering with SETD2-mediated H3K36 methylation. We propose that PRC2-mediated silencing of enhancers involved in cell differentiation represents a potential mechanism that drives these malignancies.

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Histone H3.3 G34 mutations promote aberrant PRC2 activity and drive tumor progression [ChIP-Seq]

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Imbalanced mitochondrial function provokes heterotaxy via aberrant ciliogenesis.

Project description:About 1% of all newborns are affected by congenital heart disease (CHD). Recent findings identify aberrantly functioning cilia as a possible source for CHD. Faulty cilia also prevent the development of proper left-right asymmetry and cause heterotaxy, the incorrect placement of visceral organs. Intriguingly, signaling cascades such as mTor that influence mitochondrial biogenesis also affect ciliogenesis, and can cause heterotaxy-like phenotypes in zebrafish. Here, we identify levels of mitochondrial function as a determinant for ciliogenesis and a cause for heterotaxy. We detected reduced mitochondrial DNA content in biopsies of heterotaxy patients. Manipulation of mitochondrial function revealed a reciprocal influence on ciliogenesis and affected cilia-dependent processes in zebrafish, human fibroblasts and Tetrahymena thermophila. Exome analysis of heterotaxy patients revealed an increased burden of rare damaging variants in mitochondria-associated genes as compared to 1000 Genome controls. Knockdown of such candidate genes caused cilia elongation and ciliopathy-like phenotypes in zebrafish, which could not be rescued by RNA encoding damaging rare variants identified in heterotaxy patients. Our findings suggest that ciliogenesis is coupled to the abundance and function of mitochondria. Our data further reveal disturbed mitochondrial function as an underlying cause for heterotaxy-linked CHD and provide a mechanism for unexplained phenotypes of mitochondrial disease.

| S-EPMC6597216 | biostudies-literature

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