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Deficiency of Myo18B in mice results in embryonic lethality with cardiac myofibrillar aberrations
Author(s) -
Ajima Rieko,
Akazawa Hiroshi,
Kodama Maho,
Takeshita Fumitaka,
Otsuka Ayaka,
Kohno Takashi,
Komuro Issei,
Ochiya Takahiro,
Yokota Jun
Publication year - 2008
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1111/j.1365-2443.2008.01226.x
Subject(s) - myofibril , myosin , biology , myocyte , microbiology and biotechnology , actin , cardiac myocyte , embryonic stem cell , myofilament , endocrinology , biochemistry , gene
Myo18B is an unconventional myosin family protein expressed predominantly in muscle cells. Although conventional myosins are known to be localized on the A‐bands and function as a molecular motor for muscle contraction, Myo18B protein was localized on the Z‐lines of myofibrils in striated muscles. Like Myo18A, another 18th class of myosin, the N‐terminal unique domain of the protein and not the motor domain and the coiled‐coil tail is critical for its localization to F‐actin in myocytes. Myo18B expression was induced by myogenic differentiation through the binding of myocyte‐specific enhancer factor‐2 to its promoter. Deficiency of Myo18B caused an embryonic lethality in mice accompanied by disruption of myofibrillar structures in cardiac myocytes at embryonic day 10.5. Thus, Myo18B is a unique unconventional myosin that is predominantly expressed in myocytes and whose expression is essential for the development and/or maintenance of myofibrillar structure.