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The C. elegans PH domain protein CED-12 regulates cytoskeletal reorganization via a Rho/Rac GTPase signaling pathway

Z Zhou1, E Caron, E Hartwieg

  • 1Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge 02139, USA.

Developmental Cell
|November 13, 2001
PubMed

Insights

The C. elegans gene ced-12 is crucial for clearing cellular debris and cell movement. It regulates actin cytoskeleton reorganization through conserved signaling pathways involving Rho/Rac GTPases.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • The C. elegans gene ced-12 plays a vital role in apoptotic cell engulfment and cell migration.
  • ced-12 functions in a signaling pathway with ced-2, ced-5, and ced-10 Rac GTPase, acting upstream of ced-10 Rac.
  • ced-12 encodes a protein containing a pleckstrin homology (PH) domain and an SH3 binding motif, both essential for its function.

Purpose of the Study:

  • To investigate the molecular mechanisms of CED-12 in apoptotic cell engulfment and cell migration.
  • To elucidate the role of CED-12 in regulating Rho/Rac GTPase signaling and cytoskeletal dynamics.
  • To explore the evolutionary conservation of CED-12 function.

Main Methods:

  • Genetic analysis in C. elegans to study ced-12 function in vivo.
  • Biochemical assays to investigate protein interactions, specifically CED-12 with CED-5.
  • Cellular assays in murine Swiss 3T3 fibroblasts to examine CED-12's effect on actin filament formation.

Main Results:

  • CED-12 is essential for cell corpse engulfment and cell migration in C. elegans.
  • CED-12 physically interacts with CED-5, which contains an SH3 domain.
  • Expression of CED-12 and its homologs in fibroblasts induces Rho GTPase-dependent actin filament bundle formation.

Conclusions:

  • CED-12 regulates Rho/Rac GTPase signaling, leading to cytoskeletal reorganization.
  • This regulation is mediated through interactions with cellular membranes and a CED-2/CED-5 protein complex.
  • The mechanism involving CED-12 is evolutionarily conserved across species.

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