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Noncanonical notch function in motor axon guidance is mediated by Rac GTPase and the GEF1 domain of trio
Author(s) -
Song Jeong K.,
Giniger Edward
Publication year - 2011
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.22525
Subject(s) - gtpase , guanine nucleotide exchange factor , biology , microbiology and biotechnology , axon , axon guidance , cdc42 , notch signaling pathway , abl , neuroscience , small gtpase , rac1 , signal transduction , tyrosine kinase
The receptor Notch interacts with the Abl tyrosine kinase signaling pathway to control axon growth and guidance in Drosophila motor neurons. In part, this is mediated by binding to Trio, a guanine nucleotide exchange factor (GEF) for Rho GTPases. We show here that one of the two GEF domains of Trio, the Rac‐specific GEF1, is essential for Trio‐dependent motor axon guidance and for the genetic suppression of Notch function in motor axon patterning, but the Rho‐specific GEF2 domain is not. Consistent with this, we show that Rac, and not Rho1 or Cdc42, interacts genetically with Notch in a manner indistinguishable from that of bona fide Abl signaling components. We infer, therefore, that Rac is a key component of Abl signaling in Drosophila motor axons, and specifically that it is the crucial Rho GTPase in “noncanonical” Notch/Abl signaling. Developmental Dynamics 240:324–332, 2011. © 2011 Wiley‐Liss, Inc.