| Literature DB >> 25534553 |
Hyun-Ho Kim1, Jeong-gyun Kim2, Jinkyung Jeong1, Song-Yi Han2, Kyu-Won Kim3.
Abstract
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.Entities:
Keywords: Development; Locomotion; Morphogenesis; Muscle; akap12
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Year: 2014 PMID: 25534553 DOI: 10.1016/j.diff.2014.11.002
Source DB: PubMed Journal: Differentiation ISSN: 0301-4681 Impact factor: 3.880