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Gene-environment interaction between Notch1 and oxidative stress disrupts cardiac developmental pathways

ABSTRACT: Gene-environment interaction between Notch1 and oxidative stress disrupts cardiac developmental pathways

PROVIDER: PRJNA1171854 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30954008_1.fastq.gz	Fastqsanger.gz
	SRR30954008_2.fastq.gz	Fastqsanger.gz
	SRR30954009_1.fastq.gz	Fastqsanger.gz
	SRR30954009_2.fastq.gz	Fastqsanger.gz
	SRR30954010_1.fastq.gz	Fastqsanger.gz

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Gene-environment interaction between Notch1 and oxidative stress disrupts cardiac developmental pathways

Project description:The majority of congenital heart disease cases lack a definitive cause, suggesting the role of gene-environment interactions (GxE) in disease pathogenesis. Maternal diabetes mellitus (matDM) is among the most prevalent environmental risk factors for CHD and matDM associated oxidative stress is known to disrupt cardiac development. Here, we demonstrate that NOTCH1 haploinsufficient endothelial cells have an altered transcriptomic response to oxidative stress compared to control endothelial cells, with an exacerbated effect on gene regulatory networks crucial for endocardial cushion morphogenesis.

2024-10-18 | GSE279323 | GEO

The Zmiz1-Notch1 interaction induces Myc expression to drive steady state and stress thymopoiesis [DN3]

Project description:Notch1 signaling ramps up to very high levels in order to drive CD4-CD8- double-negative (DN) thymocytes to the CD4+CD8+ double-positive (DP) stage. During this important phase of T-cell development, which is known as the DN-DP transition, it is unclear whether the Notch1 complex simply strengthens its signal output as an isolated unit or recruits cofactors to amplify its signals. We previously showed that the PIAS-like coactivator Zmiz1 is a direct and context-dependent cofactor of Notch1 in T-cell leukemia. Using conditional knockout mouse models, we show that like inactivation of Notch, inactivation of Zmiz1 impaired the DN-DP transition under steady state and stress conditions. To determine mechanism, we performed RNA-Seq on sorted DN3 cells that were deprived of Zmiz1 signals either acutely (DeltaTamCre) or chronically (DeltaMxCre). To differentiate Notch1-independent from Notch1-dependent target genes, we also performed RNA-Seq on DN3 cells that were deprived of Notch1 signals using the anti-NRR Notch1 antibody. Our data suggests that Zmiz1 selectively amplifies a subset of Notch1 target genes in DN3 cells, such as Myc.

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Genotype Environment interaction in Salmon

Project description:Genotype Environment interaction in Salmon

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Notch1

Project description:Rattus norvegicus Notch1, notch receptor 1 [Source:RGD Symbol;Acc:3187], is differentially expressed in 28 experiment(s);

| ENSRNOG00000019322 | ExpressionAtlas

Notch1

Project description:Mus musculus Notch1, notch 1 [Source:MGI Symbol;Acc:MGI:97363], is differentially expressed in 140 experiment(s);

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Notch1

Project description:Rattus norvegicus Notch1, notch receptor 1 [Source:RGD Symbol;Acc:3187], is expressed in 6 baseline experiment(s);

| ENSRNOG00000019322 | ExpressionAtlas

Notch1

Project description:Mus musculus Notch1, notch 1 [Source:MGI Symbol;Acc:MGI:97363], is expressed in 39 baseline experiment(s);

| ENSMUSG00000026923 | ExpressionAtlas

The Zmiz1-Notch1 interaction induces Myc expression to drive steady state and stress thymopoiesis [ETP and DN3]

Project description:Notch1 signaling ramps up to very high levels in order to drive CD4-CD8- double-negative (DN) thymocytes to the CD4+CD8+ double-positive (DP) stage. During this important phase of T-cell development, which is known as the DN-DP transition, it is unclear whether the Notch1 complex simply strengthens its signal output as an isolated unit or recruits cofactors to amplify its signals. We previously showed that the PIAS-like coactivator Zmiz1 is a direct and context-dependent cofactor of Notch1 in T-cell leukemia. Using conditional knockout mouse models, we show that like inactivation of Notch, inactivation of Zmiz1 impaired the DN-DP transition under steady state and stress conditions. To determine mechanism, we performed RNA-Seq on sorted early T-lineage progenitor (ETP) and DN3 cells that were deprived of Zmiz1 signals either acutely (DeltaTamCre) or chronically (DeltaMxCre). To differentiate Notch1-independent from Notch1-dependent target genes, we also performed RNA-Seq on ETP and DN3 cells that were deprived of Notch1 signals using the anti-NRR Notch1 antibody. Our data suggests that Zmiz1 selectively amplifies a subset of Notch1 target genes in DN3 cells, such as Myc. In contrast, Zmiz1 does not have these functions in ETP cells, thus indicating stage-specific roles of Zmiz1.

2018-09-21 | GSE116120 | GEO

NOTCH1

Project description:Sus scrofa NOTCH1, notch receptor 1 [Source:HGNC Symbol;Acc:HGNC:7881], is differentially expressed in 3 experiment(s);

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NOTCH1

Project description:Sus scrofa NOTCH1, notch receptor 1 [Source:HGNC Symbol;Acc:HGNC:7881], is expressed in 2 baseline experiment(s);

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