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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-2  -  Protein NMY-2

Caenorhabditis elegans

 
 
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High impact information on nmy-2

  • This result suggests that a mechanism other than cytoplasmic flow or mlc-4/nmy-2 activity can generate some a-p asymmetries in the C. elegans zygote [1].
  • Reducing the function of mlc-4 or nmy-2, a nonmuscle myosin II gene, also leads to a loss of polarized cytoplasmic flow in the C. elegans zygote, supporting models in which cytoplasmic flow may be required to establish a-p differences [1].
  • 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].
  • These phenotypes correspond to changes in the levels of phosphorylated regulatory non-muscle myosin light chain (rMLC) [3].

References

  1. The nonmuscle myosin regulatory light chain gene mlc-4 is required for cytokinesis, anterior-posterior polarity, and body morphology during Caenorhabditis elegans embryogenesis. Shelton, C.A., Carter, J.C., Ellis, G.C., Bowerman, B. J. Cell Biol. (1999) [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. Rho-binding kinase (LET-502) and myosin phosphatase (MEL-11) regulate cytokinesis in the early Caenorhabditis elegans embryo. Piekny, A.J., Mains, P.E. J. Cell. Sci. (2002) [Pubmed]
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