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Mus musculus

ABSTRACT: Identification of a regulatory domain controlling the Nppa-Nppb gene cluster during heart development and stress

PROVIDER: PRJNA327579 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3737560.fastq.gz	Fastqsanger.gz
	SRR3737561.fastq.gz	Fastqsanger.gz
	SRR3737562.fastq.gz	Fastqsanger.gz
	SRR3737563.fastq.gz	Fastqsanger.gz
	SRR3737554.fastq.gz	Fastqsanger.gz

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Identification of a regulatory domain controlling the Nppa-Nppb gene cluster during heart development and stress

Project description:The paralogous genes Nppa and Nppb are organized in an evolutionary conserved cluster and are a valuable model to study coregulation and regulatory landscape organization during heart development and disease. Here, we analyzed the chromatin conformation, epigenetic status and enhancer potential of sequences of the Nppa-Nppb cluster in vivo. Our data indicate that the regulatory landscape of the cluster is present within a 60 kbp domain centered around Nppb. Both promoters and several potential regulatory elements interact with each other in a similar manner in different tissues and developmental stages. The distribution of H3K27ac and the association of Pol2 across the locus changed during cardiac hypertrophy, revealing their potential involvement in stress-mediated gene regulation. In summary, the developmental regulation and stress-response of the Nppa-Nppb cluster involve the concerted action of multiple enhancers and epigenetic changes distributed across a structurally rigid regulatory domain. We have used 4C-seq on several viewpoints around the Nppa-Nppb gene cluster in the heart and liver samples to investigate the role of chromatin conformation on regulation of Nppa and Nppb expression during heart development and disease.

2016-07-02 | E-GEOD-81057 | biostudies-arrayexpress

Identification of a regulatory domain controlling the Nppa-Nppb gene cluster during heart development and stress

2016-07-02 | GSE81057 | GEO

Genetic dissection of a super enhancer controlling the Nppa-Nppb cluster in the heart

Project description:Genetic dissection of a super enhancer controlling the Nppa-Nppb cluster in the heart

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Genetic dissection of a super enhancer controlling the Nppa-Nppb cluster in the heart after cardiac stress

Project description:Genetic dissection of a super enhancer controlling the Nppa-Nppb cluster in the heart after cardiac stress

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Genetic dissection of a super enhancer controlling the Nppa-Nppb cluster in the heart of RE3 mutants

Project description:Genetic dissection of a super enhancer controlling the Nppa-Nppb cluster in the heart of RE3 mutants

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Genetic dissection of a super enhancer controlling the Nppa-Nppb locus in the heart (RNA-Seq)

Project description:Genetic dissection of a super enhancer controlling the Nppa-Nppb locus in the heart (RNA-Seq)

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Genetic dissection of a super enhancer controlling the Nppa-Nppb locus in the heart (CUT&RUN)

Project description:Genetic dissection of a super enhancer controlling the Nppa-Nppb locus in the heart (CUT&RUN)

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Genetic dissection of a super enhancer controlling the Nppa-Nppb locus in the heart (CUT&RUN)

Project description:CUT&RUN H3K27ac PCM-1 sorted left ventricle of Nppa-Nppb double-knockout

2020-11-25 | GSE146734 | GEO

Wnt5a-YAP signaling axis mediates mechanotransduction in cardiac myocytes and contributes to the transition to heart failure (rat sample)

Project description:Non-canonical Wnt signaling activated by Wnt5a and Wnt11 is required for the development of second heart field cardiac progenitor cells in mice. However, the pathophysiological role of non-canonical Wnt signaling in the adult heart has not been fully elucidated. Here we show that cardiomyocyte-specific Wnt5a knockout mice exhibit improved systolic function and reduced expression of mechanosensitive genes including Nppb compared to control mice when subjected to pressure overload. In cultured cardiac myocytes, Wnt5a knockdown reduces the upregulation of Nppb gene expression and YAP nuclear translocation induced by cyclic cell stretch. Wnt5a knockdown-induced Nppb downregulation in response to cell stretch is rescued by inhibition of Hippo pathway, and the rescue effect of Hippo inhibition is canceled by YAP knockdown. These results collectively suggest that Wnt5a-YAP signaling axis mediates mechanotransduction in cardiac myocytes and contributes to the transition to heart failure.

2023-07-17 | GSE200666 | GEO

Wnt5a-YAP signaling axis mediates mechanotransduction in cardiac myocytes and contributes to the transition to heart failure (mouse sample)

2023-07-17 | GSE200665 | GEO