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Transcriptional profiling of Setd5 mutant cortical tissue

ABSTRACT: Transcriptional profiling of Setd5 mutant cortical tissue

PROVIDER: PRJNA549931 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9332173_1.fastq.gz	Fastqsanger.gz
	SRR9332173_2.fastq.gz	Fastqsanger.gz
	SRR9332174_1.fastq.gz	Fastqsanger.gz
	SRR9332174_2.fastq.gz	Fastqsanger.gz
	SRR9332175_1.fastq.gz	Fastqsanger.gz

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Transcriptional profiling of Setd5 mutant cortical tissue

Project description:Setd5 inactivation in neural stem cells, zebrafish and mouse leads to a significant H3K36 hypo-methylation mostly detectable along the gene bodies. Consequently, this chromatin alteration perturbs RNA processing during elongation, compromising the transcriptional output. This gene dysregulation affects proliferative dynamics of NSCs and synaptic wiring in the neuronal derivatives, ultimately resulting in behavioral deficits in adult mice.

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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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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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Haploinsufficiency of the intellectual disability-gene SETD5 disturbs developmental gene expression and cognition

Project description:SETD5 gene mutations have been identified as a frequent cause of idiopathic intellectual disability. Here we show that Setd5 haploinsufficient mice present developmental defects such as abnormal brain to body weight ratio and neural crest defect associated phenotypes. Furthermore, Setd5 mutant mice show impairments in cognitive tasks, enhanced long-term potentiation, delayed ontogenetic profile of ultrasonic vocalisation and behavioural inflexibility. Behavioural issues are accompanied by abnormal expression of postsynaptic density proteins previously associated with cognition. Our data suggest that Setd5 might regulate RNA polymerase II dynamics and gene transcription during development and learning via its interaction with the Hdac3 and Paf1 complexes. Our results emphasize the decisive role of Setd5 in a biological pathway found to be disrupted in intellectual disability and autism spectrum disorder patients.

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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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