Coordinated lumen contraction and expansion during vulval tube morphogenesis in Caenorhabditis elegans

Dev Cell. 2012 Sep 11;23(3):494-506. doi: 10.1016/j.devcel.2012.06.019.

Abstract

Morphogenesis is a developmental phase during which cell fates are executed. Mechanical forces shaping individual cells play a key role during tissue morphogenesis. By investigating morphogenesis of the Caenorhabditis elegans hermaphrodite vulva, we show that the force-generating actomyosin network is differentially regulated by NOTCH and EGFR/RAS/MAPK signaling to shape the vulval tube. NOTCH signaling activates expression of the RHO kinase LET-502 in the secondary cell lineage through the ETS-family transcription factor LIN-1. LET-502 induces actomyosin-mediated contraction of the apical lumen in the secondary toroids, thereby generating a dorsal pushing force. In contrast, MAPK signaling in the primary lineage downregulates LET-502 RHO kinase expression to prevent toroid contraction and allow the gonadal anchor cell to expand the dorsal lumen of the primary toroids. The antagonistic action of the MAPK and NOTCH pathways thus controls vulval tube morphogenesis linking cell fate specification to morphogenesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actomyosin / metabolism
  • Animals
  • Caenorhabditis elegans / cytology
  • Caenorhabditis elegans / embryology*
  • Caenorhabditis elegans / metabolism
  • Caenorhabditis elegans Proteins / biosynthesis
  • Caenorhabditis elegans Proteins / metabolism
  • Female
  • Morphogenesis*
  • Muscle Contraction / physiology*
  • Receptors, Notch / metabolism
  • Signal Transduction
  • Vulva / cytology
  • Vulva / embryology*
  • Vulva / metabolism
  • rho-Associated Kinases / biosynthesis
  • rho-Associated Kinases / metabolism

Substances

  • Caenorhabditis elegans Proteins
  • Receptors, Notch
  • Actomyosin
  • LET-502 protein, C elegans
  • rho-Associated Kinases