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- W2090150346 abstract "Rho-binding kinase and the myosin phosphatase targeting subunit regulate nonmuscle contractile events in higher eukaryotes. Genetic evidence indicates that the C. elegans homologs regulate embryonic morphogenesis by controlling the actin-mediated epidermal cell shape changes that transform the spherical embryo into a long, thin worm. LET-502/Rho-binding kinase triggers elongation while MEL-11/myosin phosphatase targeting subunit inhibits this contractile event. We describe mutations in the nonmuscle myosin heavy chain gene nmy-1 that were isolated as suppressors of the mel-11 hypercontraction phenotype. However, a nmy-1 null allele displays elongation defects less severe than mutations in let-502 or in the single nonmuscle myosin light chain gene mlc-4. This results because nmy-1 is partially redundant with another nonmuscle myosin heavy chain, nmy-2, which was previously known only for its role in anterior/posterior polarity and cytokinesis in the early embryo. At the onset of elongation, NMY-1 forms filamentous-like structures similar to actin, and LET-502 is interspersed with these structures, where it may trigger contraction. MEL-11, which inhibits elongation, is initially cytoplasmic. In response to LET-502 activity, MEL-11 becomes sequestered away from the contractile apparatus, to the plasma membrane, when elongation commences. Upon completion of morphogenesis, MEL-11 again appears in the cytoplasm where it may halt actin/myosin contraction." @default.
- W2090150346 created "2016-06-24" @default.
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- W2090150346 date "2003-12-01" @default.
- W2090150346 modified "2023-09-26" @default.
- W2090150346 title "The<i>Caenorhabditis elegans</i>nonmuscle myosin genes<i>nmy-1</i>and<i>nmy-2</i>function as redundant components of the<i>let-502</i>/Rho-binding kinase and<i>mel-11</i>/myosin phosphatase pathway during embryonic morphogenesis" @default.
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- W2090150346 doi "https://doi.org/10.1242/dev.00807" @default.
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