2. Academic Validation
  3. CED-12/ELMO, a novel member of the CrkII/Dock180/Rac pathway, is required for phagocytosis and cell migration

CED-12/ELMO, a novel member of the CrkII/Dock180/Rac pathway, is required for phagocytosis and cell migration

  • Cell. 2001 Oct 5;107(1):27-41. doi: 10.1016/s0092-8674(01)00520-7.
T L Gumienny 1,  E Brugnera,  A C Tosello-Trampont,  J M Kinchen,  L B Haney,  K Nishiwaki,  S F Walk,  M E Nemergut,  I G Macara,  R Francis,  T Schedl,  Y Qin,  L Van Aelst,  M O Hengartner,  K S Ravichandran
Affiliations

Affiliation

  • 1 Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, NY 11743, USA.
PMID: 11595183 DOI: 10.1016/s0092-8674(01)00520-7
Abstract

The C. elegans genes ced-2, ced-5, and ced-10, and their mammalian homologs crkII, dock180, and rac1, mediate cytoskeletal rearrangements during phagocytosis of apoptotic cells and cell motility. Here, we describe an additional member of this signaling pathway, ced-12, and its mammalian homologs, elmo1 and elmo2. In C. elegans, CED-12 is required for engulfment of dying cells and for cell migrations. In mammalian cells, ELMO1 functionally cooperates with CrkII and Dock180 to promote phagocytosis and cell shape changes. CED-12/ELMO-1 binds directly to CED-5/Dock180; this evolutionarily conserved complex stimulates a Rac-GEF, leading to Rac1 activation and cytoskeletal rearrangements. These studies identify CED-12/ELMO as an upstream regulator of Rac1 that affects engulfment and cell migration from C. elegans to mammals.

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