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Mta2, a component of the NuRD complex, regulates B cell development and cooperates with OCA-B in controlling the pre-B to immature B cell transition

ABSTRACT: Mta2, a component of the NuRD complex, regulates B cell development and cooperates with OCA-B in controlling the pre-B to immature B cell transition

PROVIDER: PRJNA421876 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6365210.fastq.gz	Fastqsanger.gz
	SRR6365211.fastq.gz	Fastqsanger.gz
	SRR6365212.fastq.gz	Fastqsanger.gz
	SRR6365213.fastq.gz	Fastqsanger.gz
	SRR6365207.fastq.gz	Fastqsanger.gz

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Mta2, a component of the NuRD complex, regulates B cell development and cooperates with OCA-B in controlling the pre-B to immature B cell transition (RNA-Seq)

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Mta2, a component of the NuRD complex, regulates B cell development and cooperates with OCA-B in controlling the pre-B to immature B cell transition (RNA-Seq)

Project description:Mta2, a component of the NuRD complex, regulates B cell development and cooperates with OCA-B in controlling the pre-B to immature B cell transition (RNA-Seq)

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Mta2, a component of the NuRD complex, regulates B cell development and cooperates with OCA-B in controlling the pre-B to immature B cell transition (ChIP-Seq)

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The long non-coding RNA LINC00941 modulates MTA2/NuRD occupancy to suppress premature human epidermal differentiation

Project description:Numerous long non-coding RNAs (lncRNAs) were shown to have functional impact on cellular processes, such as human epidermal homeostasis, but for only a few the mode of action has been elucidated. Here, we report that lncRNA LINC00941 controls keratinocyte differentiation on a global level through association with the MTA2/NuRD complex, one of the major chromatin remodelers in cells. LINC00941 was found to interact with NuRD-associated MTA2, suppressing the expression of the transcription factor EGR3, a regulator of epidermal differentiation. Both LINC00941 and the MTA2/NuRD complex are enriched in non-differentiated keratinocytes and repress the expression of differentiation genes through epigenetic silencing of EGR3, consequentially preventing premature differentiation of human progenitor cells.

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Deletion of NuRD component Mta2 in nephron progenitor cells causes developmentally programmed FSGS [2month.RNAseq]

Project description:Low nephron endowment at birth is a risk factor for chronic kidney disease. The prevalence of this condition is increasing due to higher survival rates of preterm infants and children with multi- organ birth defect syndromes that affect the kidney and urinary tract. We created a mouse model of congenital low nephron number due to deletion of Mta2 in nephron progenitor cells. Mta2 is a core component of the Nucleosome Remodeling and Deacetylase (NuRD) chromatin remodeling complex. These mice developed albuminuria at 4 weeks of age followed by focal segmental glomerulosclerosis (FSGS) at 8 weeks, with progressive kidney injury and fibrosis. Our studies reveal that altered mitochondrial metabolism in the post-natal period leads to accumulation of neutral lipids in glomeruli at 4 weeks of age followed by reduced mitochondrial oxygen consumption. We found that NuRD cooperated with Zbtb7a/7b to regulate a large number of metabolic genes required for fatty acid oxidation and oxidative phosphorylation. Analysis of human kidney tissue also supported a role for reduced mitochondrial lipid metabolism and ZBTB7A/7B in FSGS and CKD. We propose that an inability to meet the physiological and metabolic demands of post-natal somatic growth of the kidney promotes the transition to CKD in the setting of glomerular hypertrophy due to low nephron endowment.

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