Zygotic loss of ZEN-4/MKLP1 results in disruption of epidermal morphogenesis in the C. elegans embryo.

نویسندگان

  • Jeff Hardin
  • Ryan King
  • Christina Thomas-Virnig
  • William B Raich
چکیده

ZEN-4/MKLP1 is required maternally for cytokinesis in Caenorhabditis elegans, but was originally identified in a screen for zygotic lethal, enclosure abnormal (Zen) mutants. We report that zen-4(w35) homozygotes exhibit stochastic failures in cytokinesis in multiple lineages. Remarkably, multinucleate epidermal cells show directional migration, even when there are as few as half the normal number of cells. Temperature shift experiments and analysis of zen-4::gfp expression confirm that the epidermal requirement for zen-4 function precedes morphogenesis. Driving expression of wild-type zen-4 by means of an epithelial-specific transgene can rescue many epidermal morphogenetic defects in zen-4 mutants. Early expression of unc-119 in epidermal precursors made this promoter unsuitable as a neuronal-specific driver in this context. Our results indicate that zygotic zen-4 function is required for correct division of epidermal precursors and, hence, indirectly for normal morphogenesis and that the epidermal morphogenetic program is surprisingly robust even in the absence of zen-4 function.

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عنوان ژورنال:
  • Developmental dynamics : an official publication of the American Association of Anatomists

دوره 237 3  شماره 

صفحات  -

تاریخ انتشار 2008