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MOG1 was initially identified as a protein that interacts with the small GTPase Ran involved in transport of macromolecules into and out of the nucleus. In addition, we have established that MOG1 interacts with the cardiac sodium channel Na v 1.5 and regulates cell surface trafficking of Na v 1.5. Here we used zebrafish as a model system to study the  in vivo  physiological role of MOG1. Knockdown of  mog1  expression in zebrafish embryos significantly decreased the heart rate (HR). Consistently, the HR increases in embryos with over-expression of human  MOG1 . Compared with wild type  MOG1  or control  EGFP , mutant  MOG1  with mutation E83D associated with Brugada syndrome significantly decreases the HR. Interestingly, knockdown of  mog1  resulted in abnormal cardiac looping during embryogenesis. Mechanistically, knockdown of  mog1  decreases expression of  hcn4  involved in the regulation of the HR, and reduces expression of  nkx2.5 ,  gata4  and  hand2  involved in cardiac morphogenesis. These data for the first time revealed a novel role that MOG1, a nucleocytoplasmic transport protein, plays in cardiac physiology and development.

Cardiac sodium channel regulator MOG1 regulates cardiac morphogenesis and rhythm