Caenorhabditis elegans genome carries two Ggamma genes
gpc-1 and
gpc-2, and two Gbeta 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 pre-exposure to the odorant,
gpc-1 mutants are still attracted to the odorant after the same pre-exposure. Cell-specific rescue experiments show that
gpc-1 acts in the AWC olfactory neurons. Co-expression 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 Ggammas 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 Ggammas. We further tested genetic interaction of
gpc-1 with several other genes involved in olfactory adaptation. Our analyses place
goa-1 Goalpha and
let-60 Ras in parallel to
gpc-1. In contrast, a gain-of-function mutation in
egl-30 Gqalpha was epistatic to
gpc-1, suggesting the possibility that
gpc-1 Ggamma may act upstream of
egl-30 Gqalpha.