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Transcriptional profiling of Setd5 heterozygous and knockout mouse embryonic stem cells

ABSTRACT: Transcriptional profiling of Setd5 heterozygous and knockout mouse embryonic stem cells

PROVIDER: PRJEB16759 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1710153_1.fastq.gz	Fastqsanger.gz
	ERR1710153_2.fastq.gz	Fastqsanger.gz
	ERR1710154_1.fastq.gz	Fastqsanger.gz
	ERR1710154_2.fastq.gz	Fastqsanger.gz
	ERR1710155_1.fastq.gz	Fastqsanger.gz

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Transcriptional profiling of Setd5 heterozygous and knockout mouse embryonic stem cells

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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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: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).

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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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Effect of Rps5 heterozygous deletion on embryonic stem cells transcriptome

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Expression data from SETD5-expressing 3T3-L1 cells.

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