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microRNA-1 (miR-1)  is an evolutionarily conserved, striated muscle-enriched miRNA. Most mammalian genomes contain two copies of miR-1, and in mice, deletion of a single locus,  miR-1-2 , causes incompletely penetrant lethality and subtle cardiac defects. Here, we report that deletion of  miR-1-1  resulted in a phenotype similar to that of the  miR-1-2  mutant. Compound  miR-1  knockout mice died uniformly before weaning due to severe cardiac dysfunction.  miR-1 -null cardiomyocytes had abnormal sarcomere organization and decreased phosphorylation of the regulatory myosin light chain-2 (MLC2), a critical cytoskeletal regulator. The smooth muscle-restricted inhibitor of MLC2 phosphorylation, Telokin, was ectopically expressed in the myocardium, along with other smooth muscle genes.  miR-1  repressed Telokin expression through direct targeting and by repressing its transcriptional regulator, Myocardin. Our results reveal that  miR-1  is required for postnatal cardiac function and reinforces the striated muscle phenotype by regulating both transcriptional and effector nodes of the smooth muscle gene expression network.

microRNA-1 regulates sarcomere formation and suppresses smooth muscle gene expression in the mammalian heart