Akap12 is essential for the morphogenesis of muscles involved in zebrafish locomotion

• Loss of akap12 function causes severe defects in locomotor activity in zebrafish embryos.
• Slow muscle cells lacking akap12 failed to migrate laterally and remained deep within the myotome.
• Muscle pioneers showed aberrant migration to the superficial layer of the myotome in the akap12 morphants.
• Such defects in akap12 morphants resulted from a direct effect within the slow muscle and muscle pioneer cells.

Swimming behavior in fish is driven by coordinated contractions of muscle fibers. In zebrafish, slow muscle cell migration is crucial for the formation of the muscle network; slow myoblasts, which arise from medial adaxial cells, migrate radially to the lateral surface of the trunk and tail during embryogenesis. This study found that the zebrafish A-kinase anchoring protein (akap)12 isoforms akap12α and akap12β are required for muscle morphogenesis and locomotor activity. Embryos deficient in akap12 exhibited reduced spontaneous coiling, touch response, and free swimming. Akap12-depleted slow but not fast muscle cells were misaligned, suggesting that the behavioral abnormalities resulted from specific defects in slow muscle patterning; indeed, slow muscle cells and muscle pioneers in these embryos showed abnormal migration in a cell-autonomous manner. Taken together, these results suggest that akap12 plays a critical role in the development of zebrafish locomotion by regulating the normal morphogenesis of muscles.