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SETD5 is a H3K36 methyltransferase which preserves transcriptional fidelity during brain development and neuronal wiring [RNA-seq]

ABSTRACT: We assess the role of Setd5 on trancription elongation, by profiling nascent chromatin bound RNAs after DRB treatment an release, in wild type and Setd5 heterozygous mouse neural stem cells (NSCs).

ORGANISM(S): Mus musculus

PROVIDER: GSE127004 | GEO | 2019/07/10

REPOSITORIES: GEO

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SETD5 is a H3K36 methyltransferase which preserves transcriptional fidelity during brain development and neuronal wiring [ChIP-seq]

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SETD5 is a H3K36 methyltransferase which preserves transcriptional fidelity during brain development and neuronal wiring

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SETD5 is a H3K36 methyltransferase which preserves transcriptional fidelity during brain development and neuronal wiring

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Project description:SETD5 is a H3K36 methyltransferase which preserves transcriptional fidelity during brain development and neuronal wiring [ChIP-seq]

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SETD5 is a H3K36 methyltransferase which preserves transcriptional fidelity during brain development and neuronal wiring [RNA-seq]

Project description:SETD5 is a H3K36 methyltransferase which preserves transcriptional fidelity during brain development and neuronal wiring [RNA-seq]

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Project description:SET-domain containing proteins play a vital role in regulating gene expression during development through modifications in chromatin structure. To study molecular function of SET domain containing 5 (Setd5), we assessed global changes in the mouse embryonic stem cell transcriptome when Setd5 gene is knocked out.

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Project description:Neurodevelopmental disorders (NDDs) are heterogeneous conditions due to alterations of a variety of molecular mechanisms and cell dysfunctions. Epigenetic basis of NDDs have been reported in an increasingly number of cases while mitochondrial dysfunctions are more common within NDD patients than in the general population. Here, we investigated experimental models of Setd5 haploinsufficiency, that leads to NDDs in humans due to chromatin defects, and uncovered that mitochondrial dysfunction participates in the pathogenesis. Mitochondrial impairment is facilitated by transcriptional aberrations that follow the decrease of SETD5 enzyme. Low levels of SETD5 resulted in fragmented mitochondria, less mitochondrial potential and ATP production both in neural precursors and neurons. Mitochondria were miss-localized in mutant neurons, with few organelles within neurites and synapses. Our study explores the epigenetics/mitochondria interplay as an important aspect of NDD pathophysiology and defines the impairments of mitochondrial functionality and dynamics as new therapeutic targets for disorders associated with loss of SETD5.

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