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Originally published as Genetics Published Articles Ahead of Print on February 2, 2009.
Genetics, Vol. 181, 1347-1357, April 2009, Copyright © 2009
doi:10.1534/genetics.108.099002
GPC-1, a G Protein
-Subunit, Regulates Olfactory Adaptation in Caenorhabditis elegans
Koji Yamada*,
Takaaki Hirotsu
,
Masahiro Matsuki
,1,
Hirofumi Kunitomo
and
Yuichi Iino*,2
* Department of Biophysics and Biochemistry,
Molecular Genetics Research Laboratory, Graduate School of Science, The University of Tokyo, Tokyo 113-0033, Japan and
Department of Biology, Graduate School of Science, Kyushu University, Fukuoka 812-8581, Japan
2 Corresponding address: Department of Biophysics and Biochemistry, Graduate School of Science, The University of Tokyo, Science Building 7, Room 603, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.
E-mail: iino{at}biochem.s.u-tokyo.ac.jp
Caenorhabditis elegans genome carries two G
genes, gpc-1 and gpc-2, and two Gβ genes, gpb-1 and gpb-2. Of these, gpc-2 and gpb-1 are expressed ubiquitously and are essential for viability. Through a genetic screen, we identified gpc-1 as essential for olfactory adaptation. While wild-type animals show decreased chemotaxis to the odorant benzaldehyde after a short preexposure to the odorant, gpc-1 mutants are still attracted to the odorant after the same preexposure. Cell-specific rescue experiments show that gpc-1 acts in the AWC olfactory neurons. Coexpression of GPC-1 and GPB-1, but not GPB-2, caused enhanced adaptation, indicating that GPC-1 may act with GPB-1. On the other hand, knock down of gpc-2 by cell-targeted RNAi caused reduced chemotaxis to the odorant in unadapted animals, indicating that GPC-2 mainly act for olfactory sensation and the two G
's have differential functions. Nonetheless, overexpression of gpc-2 in AWC neurons rescued the adaptation defects of gpc-1 mutants, suggesting partially overlapping functions of the two G
's. We further tested genetic interaction of gpc-1 with several other genes involved in olfactory adaptation. Our analyses place goa-1 Go
and let-60 Ras in parallel to gpc-1. In contrast, a gain-of-function mutation in egl-30 Gq
was epistatic to gpc-1, suggesting the possibility that gpc-1 G
may act upstream of egl-30 Gq
.