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

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

PROVIDER: PRJNA1034138 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26621450_1.fastq.gz	Fastqsanger.gz
	SRR26621450_2.fastq.gz	Fastqsanger.gz
	SRR26621451_1.fastq.gz	Fastqsanger.gz
	SRR26621451_2.fastq.gz	Fastqsanger.gz
	SRR26621452_1.fastq.gz	Fastqsanger.gz

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

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.

2023-11-05 | GSE246693 | GEO

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

2023-11-05 | GSE246692 | GEO

Deletion of NuRD component Mta2 in nephron progenitor cells causes developmentally programmed FSGS [E17.RNAseq]

2023-11-05 | GSE246694 | GEO

Deletion of NuRD component Mta2 in nephron progenitor cells causes developmentally programmed FSGS

Project description:Deletion of NuRD component Mta2 in nephron progenitor cells causes developmentally programmed FSGS

| PRJNA1034132 | ENA

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

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

| PRJNA1034139 | ENA

Deletion of NuRD component Mta2 in nephron progenitor cells causes developmentally programmed FSGS [E17.RNAseq]

Project description:Deletion of NuRD component Mta2 in nephron progenitor cells causes developmentally programmed FSGS [E17.RNAseq]

| PRJNA1034137 | ENA

Deletion of NuRD component Mta2 in nephron progenitor cells causes developmentally programmed FSGS

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-11-05 | GSE246695 | GEO

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.

2024-04-08 | PXD043838 | Pride

The long non-coding RNA LINC00941 regulates human epidermal homeostasis through interaction with the MTA2/NuRD complex

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 repressing premature differentiation of human progenitor cells.

2024-04-08 | GSE237175 | GEO

The NuRD complex suppresses transcriptional noise during lineage commitment [ChIP-Seq]

Project description:Here we set out to define the biochemical and functional diversity encoded by one such group of proteins within the mammalian Nucleosome Remodelling and Deacetylation (NuRD) complex: Mta1, Mta2 and Mta3. We find that, in contrast to what has been described in somatic cells, MTA proteins are not mutually exclusive within ES cell NuRD and, despite subtle differences in chromatin binding and biochemical interactions, serve largely redundant functions. ES cells lacking all three MTA proteins represent a complete NuRD null and are viable, allowing us to identify a highly previously unreported function for NuRD in reducing transcriptional noise, which is essential for maintaining a proper differentiation trajectory during early stages of lineage commitment.

2019-04-17 | GSE122830 | GEO

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