title: The Drosophila GIPC homologue can modulate myosin based processes and planar cell polarity but is not essential for development.
abstract: Epithelia often show, in addition to the ubiquitous apico-basal (A/B) axis, a polarization within the plane of the epithelium, perpendicular to the A/B axis. Such planar cell polarity (PCP) is for example evident in the regular arrangement of the stereocilia in the cochlea of the mammalian inner ear or in (almost) all Drosophila adult external structures. GIPCs (GAIP interacting protein, C terminus) were first identified in mammals and bind to the Galphai GTPase activating protein RGS-GAIP. They have been proposed to act in a G-protein coupled complex controlling vesicular trafficking. Although GIPCs have been found to bind to numerous proteins including Frizzled receptors, which participate in PCP establishment, there is little in vivo evidence for the functional role(s) of GIPCs. We show here that overexpressed Drosophila dGIPC alters PCP generation in the wing. We were however unable to find any binding between dGIPC and the Drosophila receptors Fz1 and Fz2. The effect of overexpressed dGIPC is likely due to an effect on the actin cytoskeleton via myosins, since it is almost entirely suppressed by removing a genomic copy of the Myosin VI/jaguar gene. Surprisingly, although dGIPC can interfere with PCP generation and myosin based processes, the complete loss-of-function of dGIPC gives viable adults with no PCP or other detectable defects arguing for a non-essential role of dGIPC in viability and normal Drosophila development.
authors.affiliation: Department of Physiology Development and Neuroscience, University of Cambridge, Cambridge, UK.
authors.forename: Alexandre
authors.initials: A
authors.lastname: Djiane
authors.forename: Marek
authors.initials: M
authors.lastname: Mlodzik
mesh_terms: D000199:Actins / Q000378:metabolism; D000818:Animals; D002352:Carrier Proteins / Q000737:chemistry / Q000235:genetics / Q000378:metabolism*; D016764:Cell Polarity; D003599:Cytoskeleton / Q000378:metabolism; D029721:Drosophila Proteins / Q000737:chemistry / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D004331:Drosophila melanogaster / Q000166:cytology* / Q000235:genetics / Q000254:growth & development / Q000378:metabolism*; D005260:Female; D005786:Gene Expression Regulation; D008297:Male; D008565:Membrane Proteins / Q000235:genetics; D018995:Myosin Heavy Chains / Q000235:genetics; D009218:Myosins / Q000235:genetics / Q000378:metabolism*; D017384:Sequence Deletion; D017386:Sequence Homology, Amino Acid; D014921:Wings, Animal / Q000166:cytology / Q000378:metabolism
chemical_list: D000199:Actins; D002352:Carrier Proteins; D029721:Drosophila Proteins; D008565:Membrane Proteins; C097862:Zip protein, Drosophila; C553161:kermit protein, Drosophila; C089785:myosin VI; D018995:Myosin Heavy Chains; D009218:Myosins