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TETs Regulate Proepicardial Cell Migration through Extracellular Matrix Organization during Zebrafish Cardiogenesis

ABSTRACT: TETs Regulate Proepicardial Cell Migration through Extracellular Matrix Organization during Zebrafish Cardiogenesis

PROVIDER: PRJNA501891 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8137050_1.fastq.gz	Fastqsanger.gz
	SRR8137050_2.fastq.gz	Fastqsanger.gz
	SRR8137051_1.fastq.gz	Fastqsanger.gz
	SRR8137051_2.fastq.gz	Fastqsanger.gz
	SRR8137042_1.fastq.gz	Fastqsanger.gz

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TETs Regulate Proepicardial Cell Migration through Extracellular Matrix Organization during Zebrafish Cardiogenesis.

Project description:Ten-eleven translocation (Tet) enzymes (Tet1/2/3) mediate 5-methylcytosine (5mC) hydroxylation, which can facilitate DNA demethylation and thereby impact gene expression. Studied mostly for how mutant isoforms impact cancer, the normal roles for Tet enzymes during organogenesis are largely unknown. By analyzing compound mutant zebrafish, we discovered a requirement for Tet2/3 activity in the embryonic heart for recruitment of epicardial progenitors, associated with development of the atrial-ventricular canal (AVC). Through a combination of methylation, hydroxymethylation, and transcript profiling, the genes encoding the activin A subunit Inhbaa (in endocardium) and Sox9b (in myocardium) were implicated as demethylation targets of Tet2/3 and critical for organization of AVC-localized extracellular matrix (ECM), facilitating migration of epicardial progenitors onto the developing heart tube. This study elucidates essential DNA demethylation modifications that govern gene expression changes during cardiac development with striking temporal and lineage specificities, highlighting complex interactions in multiple cell populations during development of the vertebrate heart.

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TETs Regulate Proepicardial Cell Migration through Extracellular Matrix Organization during Zebrafish Cardiogenesis

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Ablation of collagen XII disturbs joint extracellular matrix organization and causes patellar subluxation

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Project description:Chronic pain is a debilitating and poorly-treated condition. The mechanisms underlying the development of chronic pain are not well understood. Nerve injury and inflammation cause alterations in gene expression in tissues associated with transmission of pain, supporting molecular and cellular mechanisms that maintain painful states. Previous studies in animal models and human patients suffering from different chronic pain conditions have examined changes in transcriptome associated with chronic pain. However, in most studies, the analyses were restricted to a single tissue or pain condition. In the current study, we performed next-generation sequencing of dorsal root ganglia, spinal cord, brain and blood in mouse models of nerve injury and inflammation-induced chronic pain. Comparative analyses of differentially expressed genes (DEG) across these tissues in two pain models identified the extracellular matrix organization (ECMO) pathway as the most commonly affected pathway. Interestingly, examination of GWAS datasets revealed an over-representation of DEGs within the ECMO pathway in SNPs most strongly associated with human back pain. Remarkably, manipulation of the extracellular matrix in the mouse significantly affected the development of pain hypersensitivity following nerve injury, supporting our gene expression findings. In summary, our comprehensive analysis of transcriptional landscape across different mouse pain models and tissues as well as human GWAS datasets identified extracellular matrix organization as a central molecular pathway in the development of chronic pain.

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