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Gene regulation of PHF6 in mouse developing cortex

ABSTRACT: Gene regulation of PHF6 in mouse developing cortex

PROVIDER: PRJNA490879 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7829930.fastq.gz	Fastqsanger.gz
	SRR7829940.fastq.gz	Fastqsanger.gz
	SRR7829931.fastq.gz	Fastqsanger.gz
	SRR7829941.fastq.gz	Fastqsanger.gz
	SRR7829932.fastq.gz	Fastqsanger.gz

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Gene regulation of PHF6 in mouse developing cortex

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Project description:The plant homeodomain zinc finger protein,PHF6, is a transcriptional regulator, with its germline mutations causing the X-linked intellectual disability (XLID), Börjeson-Forssman-Lehmann syndrome (BFLS).The precise mechanisms by whichPHF6regulates transcription and how its mutant forms lead to XLID remain poorly characterized. Here, we show genome-wide binding of PHF6 in the developing cortex, most of which overlap (CA)n-microsatellite repeats near genes involved in central nervous system development and neurogenesis. Mice harbouring BFLS patient mutations exhibit defects in neurogenesis and altered neural stem cell fate. Mechanistically, we find that PHF6 regulatesa panel of Ephrin receptors (EphRs)and that PHF6regulation ofEphRis impaired in BFLS mice and ina conditionalPhf6knock-out mouse model. We report that mice harboring BFLS mutations exhibit an increase in embryonic neural stem cell (eNSC) self-renewal, a significant attenuation of newly born neurons, and thatEphRknockdown phenocopies the PHF6 loss-of-function defects in altering eNSC fate. Our results suggest that alterations in eNSC fate specification via a PHF6/EphRtranscriptional pathway leads to impaired neurogenesis in BFLS

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Project description:Loss-of-function mutations Phf6 occur frequently in both adult and pediatric T-cell Acute Lymphoblastic Leukemia (T-ALL). Although Phf6 is widely expressed, little is known about its proposed function as epigenetic regulator and tumor suppressor. To address the role of Phf6 in the leukemia development, here we analyze by RNAseq the gene expression profiles of isogenic Phf6 wild type and Phf6 knockout leukemia cells transformed by overexpression of an oncogenic mutant form of the NOTCH1 receptor.

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Developing mouse embryo

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2024-11-15 | GSE281625 | GEO

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