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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Gene Review: 

nmy-1  -  Protein NMY-1

Caenorhabditis elegans

 
 
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High impact information on myosin

  • Loss of RHO-1 activity causes defects in the early organization of the myosin cytoskeleton but does not inhibit segregation of myosin to the anterior [1].
  • We describe mutations in the nonmuscle myosin heavy chain gene nmy-1 that were isolated as suppressors of the mel-11 hypercontraction phenotype [2].
  • Upon completion of morphogenesis, MEL-11 again appears in the cytoplasm where it may halt actin/myosin contraction [2].
  • 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 [2].
 

Associations of myosin with chemical compounds

References

  1. CDC-42 and RHO-1 coordinate acto-myosin contractility and PAR protein localization during polarity establishment in C. elegans embryos. Schonegg, S., Hyman, A.A. Development (2006) [Pubmed]
  2. The Caenorhabditis elegans nonmuscle myosin genes nmy-1 and nmy-2 function as redundant components of the let-502/Rho-binding kinase and mel-11/myosin phosphatase pathway during embryonic morphogenesis. Piekny, A.J., Johnson, J.L., Cham, G.D., Mains, P.E. Development (2003) [Pubmed]
  3. Caenorhabditis elegans kettin, a large immunoglobulin-like repeat protein, binds to filamentous actin and provides mechanical stability to the contractile apparatuses in body wall muscle. Ono, K., Yu, R., Mohri, K., Ono, S. Mol. Biol. Cell (2006) [Pubmed]
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