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

ABSTRACT: We assess the epigenetic function of Setd5 in mouse neural stem cells (NSCs), by profiling a panel of histone modifications and Setd5 binding in wild type and Setd5 heterozygous NSCs.

ORGANISM(S): Mus musculus

PROVIDER: GSE104274 | 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 [RNA-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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SETD5 is a H3K36 methyltransferase which preserves transcriptional fidelity during brain development and neuronal wiring [ChIP-seq]

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Transcriptional profiling of Setd5 mutant cortical tissue

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Setd5 haploinsufficiency alters neuronal network connectivity and leads to autistic-like behaviors in mice [bulk RNA]

Project description:SETD5, a gene linked to intellectual disability (ID) and autism spectrum disorder (ASD), is a member of the SET-domain family and encodes a putative histone methyltransferase (HMT). To date, the mechanism by which SETD5 haploinsufficiency causes ASD/ID remains an unanswered question. Setd5 is the highly conserved mouse homolog, and although the Setd5 null mouse is embryonic lethal, the heterozygote is viable. Morphological tracing and multi electrode array was used on cultured cortical neurons. MRI was conducted of adult mouse brains and immunohistochemistry of juvenile mouse brains. RNA-Seq was used to investigate gene expression in the developing cortex. Behavioral assays were conducted on adult mice. Setd5+/- cortical neurons displayed significantly reduced synaptic density and neuritic outgrowth in vitro, with corresponding decreases in network activity and synchrony by electrophysiology. A specific subpopulation of fetal Setd5+/- cortical neurons showed altered gene expression of neurodevelopment-related genes. Setd5+/- animals manifested several autism-like behaviors, including hyperactivity, cognitive deficit, and altered social interactions. Anatomical differences were observed in Setd5+/- adult brains, accompanied by a deficit of deep-layer cortical neurons in the developing brain. Our data converge on a picture of abnormal neurodevelopment driven by Setd5 haploinsufficiency, consistent with a highly penetrant risk factor.

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Transcriptional profiling of Setd5 heterozygous and knockout mouse embryonic stem cells

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