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First published online 25 February 2009
doi: 10.1242/dev.026666

Development 136, 1201-1210 (2009)
Published by The Company of Biologists 2009
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C. elegans CARMIL negatively regulates UNC-73/Trio function during neuronal development

Pamela J. Vanderzalm1,*, Amita Pandey1, Michael E. Hurwitz2,3, Laird Bloom2,{dagger}, H. Robert Horvitz2 and Gian Garriga1,4,{ddagger}

1 Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA.
2 Howard Hughes Medical Institute and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
3 Massachusetts General Hospital Cancer Center, Department of Medicine, Massachusetts General Hospital, Boston, MA 02114, USA.
4 Helen Wills Neuroscience Institute, University of California, Berkeley, CA 94720, USA.

{ddagger} Author for correspondence (e-mail: garriga{at}berkeley.edu)

Accepted 2 February 2009

Whereas many molecules that promote cell and axonal growth cone migrations have been identified, few are known to inhibit these processes. In genetic screens designed to identify molecules that negatively regulate such migrations, we identified CRML-1, the C. elegans homolog of CARMIL. Although mammalian CARMIL acts to promote the migration of glioblastoma cells, we found that CRML-1 acts as a negative regulator of neuronal cell and axon growth cone migrations. Genetic evidence indicates that CRML-1 regulates these migrations by inhibiting the Rac GEF activity of UNC-73, a homolog of the Rac and Rho GEF Trio. The antagonistic effects of CRML-1 and UNC-73 can control the direction of growth cone migration by regulating the levels of the SAX-3 (a Robo homolog) guidance receptor. Consistent with the hypothesis that CRML-1 negatively regulates UNC-73 activity, these two proteins form a complex in vivo. Based on these observations, we propose a role for CRML-1 as a novel regulator of cell and axon migrations that acts through inhibition of Rac signaling.

Key words: Cell migration, Axon guidance, Rac GTPase, CARMIL (Lrrc16a), Trio, Robo


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