PMC

GPB-1, but not GPB-2, may function with both GPC-1 and GPC-2 in olfactory adaptation. (A) The expression of gpc-1, gpb-1, or gpb-2 in AWC sensory neurons using the odr-3 promoter does not affect the olfactory adaptation of wild-type animals significantly (P > 0.01). Enhanced adaptation was observed only when gpb-1 and gpc-1 were co-overexpressed in AWC sensory neurons. (B) The expression of gpc-2 in AWC sensory neurons fully rescues the olfactory adaptation defect of gpc-1(pe372) animals. **P < 0.001.

Properties of olfactory adaptation and chemotaxis of wild-type animals and gpc-1 mutant animals. (A) Olfactory adaptation of wild-type, gpc-1(pe372), and gpc-1(pk298) animals. Worms were treated with 5 min of preexposure with basal buffer (open bars) or benzaldehyde (100 nl/ml; solid bars) and assayed for chemotaxis. Both pe372 and pk298 mutants are defective in olfactory adaptation. (B) Chemotaxis of untreated wild-type and pe372 animals to different concentrations of benzaldehyde. pe372 animals respond normally to a wide range of concentrations. (C) Olfactory adaptation assays with various durations of preexposure. Basal buffer (dotted lines), and benzaldehyde (100 nl/ml; solid lines). pe372 animals adapt to benzaldehyde weakly compared to wild-type animals. **P < 0.001; *P < 0.01.

Excessive activation of EGL-30 G_qα and elevated DAG signals inhibit olfactory adaptation. (A) Adaptation of wild-type animals, egl-30(js126) mutants, syIs36[egl-30(+)] animals, and wild-type animals carrying odr-1p::egl-30(Q205L) transgene to benzaldehyde. All mutants are defective for adaptation. (B) Wild-type animals treated with phorbol ester PMA (0.5 μg/ml) show a severe adaptation defect. (C) Adaptation of eat-16 mutants, gpb-2 mutants, and animals carrying a high-copy egl-10 array to benzaldehyde. eat-16 mutants and egl-10-overexpressing animals show a modest defect, and gpb-2 mutants exhibit a slight defect in adaptation. (D) Overexpression of the egl-10 gene in gpb-2 mutants hardly causes an additive defect in olfactory adaptation. Chemotaxis indices of two transgenic lines were averaged. *, P < 0.001; +, P < 0.01.

GOA-1 G_oα appears to antagonize the EGL-30 G_qα–DAG signaling pathway by down-regulation of EGL-30 G_qα in olfactory adaptation. (A) Adaptation of DGK mutants to benzaldehyde. dgk-3; dgk-1 double mutants show a defect in adaptation. (B) Adaptation defect observed in dgk-3; dgk-1 double mutants is suppressed by the expression of goa-1(Q205L) in AWC chemosensory neurons. (C) Adaptation defects observed in eat-16(ce71) and gpb-2(vs23) mutants are suppressed by the expression of goa-1(Q205L) in AWC chemosensory neurons. (D) GOA-1 may act upstream of EGL-30 in olfactory adaptation. Animals carrying odr-1p::goa-1(Q205L) were crossed to animals carrying odr-1p::egl-30(Q205L) to generate animals carrying both constructs. There is no significant difference between responses of animals expressing both constructs and that of animals expressing only egl-30(Q205L) after preexposure to weak (gray bars) or normal benzaldehyde (black bars) (P = 0.04 or P = 0.79, respectively). However, the expression of goa-1(Q205L) in AWC neurons inhibits chemotaxis, even if egl-30(Q205L) is expressed together (white bars). *, P < 0.001; +, P < 0.01.