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. 2008 Oct 13;105(42):16350–16355. doi: 10.1073/pnas.0803617105

Fig. 4.

Fig. 4.

aex genes likely regulate the defecation through downstream Gsα and adenylyl cyclase signaling and GABAergic neuron activation. (A) Gain-of-function allele of Gsα [gsa-1(ce81)] completely suppresses the Exp defects in aex-2 mutants. In contrast, a gain-of-function in Gqα [egl-30(js126)] and a loss-of-function [dgk-1(sy428)] that phenocopies egl-30 gain-of-function have only mild effects on the aex-2 Exp defects. When an activated adenylyl cyclase gene [acy-1(js127)] is specifically expressed in the GABAergic neurons, it significantly suppresses the Exp defects of aex-2, aex-4, and aex-5 mutants. (B) Activation of GABAergic neurons by photoactivatable ChR2 suppresses the Exp defects in aex mutants. The photoactivatable cation channel ChR2 was expressed specifically in GABAergic neurons under the Punc-47 promoter in aex-2, aex-4, and aex-5 mutants. In the presence of all-trans retinal and blue-light activation, the ChR2 fully suppresses the Exp defects in all the aex mutants. In contrast, in the absence of all-trans retinal or blue light, the ChR2 transgene does not rescue the defecation mutant phenotypes to WT levels. *, P < 0.05; **, P < 0.005; ***, P < 0.0005 significantly different from the respective mutant. +, P > 0.05 not significantly different from WT. Error bars represent SEM. See SI Text for transgenes and clones.