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MicroRNA 19a replacement partially rescues fin and cardiac defects in zebrafish model of Holt Oram syndrome [array]

ABSTRACT: The regulative role of miRNAs in Holt-Oram Syndrome is investigated in a zebrafish model.

ORGANISM(S): Danio rerio

PROVIDER: GSE69578 | GEO | 2015/10/01

SECONDARY ACCESSION(S): PRJNA285897

REPOSITORIES: GEO

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MicroRNA 19a replacement partially rescues fin and cardiac defects in zebrafish model of Holt Oram syndrome [miRNA-seq]

Project description:The regulative role of miRNAs in Holt-Oram Syndrome is investigated in a zebrafish model.

2015-10-01 | GSE69690 | GEO

MicroRNA 19a replacement partially rescues fin and cardiac defects in zebrafish model of Holt Oram syndrome.

Project description:Holt-Oram Syndrome (HOS) is an autosomal dominant heart-hand syndrome caused by mutations in the TBX5 gene, a transcription factor capable of regulating hundreds of cardiac-specific genes through complex transcriptional networks. Here we show that, in zebrafish, modulation of a single miRNA is sufficient to rescue the morphogenetic defects generated by HOS. The analysis of miRNA-seq profiling revealed a decreased expression of miR-19a in Tbx5-depleted zebrafish embryos compared to the wild type. We revealed that the transcription of the miR-17-92 cluster, which harbors miR-19a, is induced by Tbx5 and that a defined dosage of miR-19a is essential for the correct development of the heart. Importantly, we highlighted that miR-19a replacement is able to rescue cardiac and pectoral fin defects and to increase the viability of HOS zebrafish embryos. We further observed that miR-19a replacement shifts the global gene expression profile of HOS-like zebrafish embryos towards the wild type condition, confirming the ability of miR-19a to rescue the Tbx5 phenotype. In conclusion our data demonstrate the importance of Tbx5/miR-19a regulatory circuit in heart development and provide a proof of principle that morphogenetic defects associated with HOS can be rescued by transient miRNA modulation.

| S-EPMC4677400 | biostudies-literature

MicroRNA 19a replacement partially rescues fin and cardiac defects in zebrafish model of Holt Oram syndrome

Project description:MicroRNA 19a replacement partially rescues fin and cardiac defects in zebrafish model of Holt Oram syndrome

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MicroRNA 19a replacement partially rescues fin and cardiac defects in zebrafish model of Holt Oram syndrome

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

2015-10-01 | GSE69691 | GEO

Holt-Oram syndrome at single cell resolution

Project description:Holt-Oram syndrome (HOS), characterized by heart and forelimb defects, is caused by mutations in the T-box transcription factor, TBX5. While much has been done to elucidate TBX5’s transcriptional mechanisms in animal and human induced pluripotent stem cell (iPSC) models, transcriptomics from HOS patient tissue is lacking.

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Discovering miRNA regulatory networks in Holt-Oram Syndrome using a Zebrafish model [array]

Project description:To investigate the complex regulatory networks disrupted in Holt-Oram Syndrome, we characterized genome-widely the miRNA and mRNA expression profiles in WT and Tbx5 depleted zebrafish embryos at two development time points, 24 and 48 hpf.

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Holt-Oram syndrome at single cell resolution

Project description:Holt-Oram syndrome at single cell resolution

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Discovering miRNA regulatory networks in Holt-Oram Syndrome using a Zebrafish model [miRNA-seq]

2016-04-24 | GSE64465 | GEO

Discovering miRNA regulatory networks in Holt-Oram Syndrome using a Zebrafish model

Project description:Discovering miRNA regulatory networks in Holt-Oram Syndrome using a Zebrafish model

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Holt-Oram Syndrome With Multiple Cardiac Abnormalities.

Project description:Holt-Oram syndrome (HOS) is a rare monogenic disorder characterized by upper limb abnormalities, congenital heart defects and/or conduction abnormalities. It is determined by mutations of TBX5 gene and is inherited in an autosomal dominant manner. Penetrance is complete, but variable expressivity is present, which gives sometimes diagnostic difficulties. Our case is a young adult with a personal history of preaxial polydactyly operated in infancy, multiple cardiac malformations (atrial septal defect, bicuspid aortic valve, left ventricular non-compaction) and radiologic findings consistent with HOS. Family history is negative for HOS. In conclusion, we present a case of HOS diagnosed in the adult period to highlight the diagnostic problems for the proband and the family and the importance of an early diagnostic.

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