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However, the in vivo physiological role of <jats:italic>mog1<\/jats:italic> in the heart needs to be fully defined.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p><jats:italic>Mog1<\/jats:italic> knockout zebrafish was generated by TALEN. Echocardiography, histological analysis, and electrocardiograms were used to examine cardiac structure and function. RNA sequencing and real\u2010time RT\u2010PCR were used to elucidate the molecular mechanism and to analyse the gene expression. Isoproterenol was used to induce cardiac hypertrophy. Whole\u2010mount in situ hybridization was used to observe cardiac morphogenesis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p><jats:italic>Mog1<\/jats:italic> knockout zebrafish developed cardiac hypertrophy and heart failure (enlarged pericardium, increased <jats:italic>nppa<\/jats:italic> and <jats:italic>nppb<\/jats:italic> expression and ventricular wall thickness, and reduced ejection fraction), which was aggravated by isoproterenol. RNAseq and KEGG pathway analyses revealed the effect of <jats:italic>mog1<\/jats:italic> knockout on the pathways of cardiac hypertrophy, dilatation and contraction. Mechanistic studies revealed that <jats:italic>mog1<\/jats:italic> knockout decreased expression of <jats:italic>tbx5<\/jats:italic>, which reduced expression of <jats:italic>cryab<\/jats:italic> and <jats:italic>hspb2<\/jats:italic>, resulting in cardiac hypertrophy and heart failure. Overexpression of <jats:italic>cryab<\/jats:italic>, <jats:italic>hspb2<\/jats:italic> and <jats:italic>tbx5<\/jats:italic> rescued the cardiac oedema phenotype of <jats:italic>mog1<\/jats:italic> KO zebrafish. Telemetry electrocardiogram monitoring showed QRS and QTc prolongation and a reduced heart rate in <jats:italic>mog1<\/jats:italic> knockout zebrafish, which was associated with reduced <jats:italic>scn1b<\/jats:italic> expression. Moreover, <jats:italic>mog1<\/jats:italic> knockout resulted in abnormal cardiac looping during embryogenesis because of the reduced expression of <jats:italic>nkx2.5<\/jats:italic>, <jats:italic>gata4<\/jats:italic> and <jats:italic>hand2<\/jats:italic>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Our data identified an important molecular determinant for cardiac hypertrophy and heart failure, and rhythm maintenance of the heart.<\/jats:p><\/jats:sec>","DOI":"10.1111\/apha.13567","type":"journal-article","created":{"date-parts":[[2020,10,8]],"date-time":"2020-10-08T21:59:35Z","timestamp":1602194375000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["<i>Mog1<\/i> knockout causes cardiac hypertrophy and heart failure by downregulating <i>tbx5\u2010cryab\u2010hspb2<\/i> signalling in zebrafish"],"prefix":"10.1111","volume":"231","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7458-0787","authenticated-orcid":false,"given":"Dongzhi","family":"Gou","sequence":"first","affiliation":[{"name":"Key Laboratory of Molecular Biophysics of the Ministry of Education College of Life Science and Technology and Center for Human Genome Research Huazhong University of Science and Technology Wuhan P. 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