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. 2013 Jul 11;9(7):e1003619. doi: 10.1371/journal.pgen.1003619

Figure 5. Guanylyl cyclases act upstream of EGL-4.

Figure 5

(A) The osm-10 promoter [3] was used to express wild-type EGL-4 or the cGMP binding mutant EGL-4(T276A) in the ASH sensory neurons of egl-4(lof) animals. While wild-type EGL-4 significantly rescued the egl-4(lof) quinine hypersensitivity (p<0.001), egl-4(lof) animals expressing EGL-4(T276A) remained hypersensitive. (B) Loss-of-function mutations in the guanylyl cyclase genes odr-1, gcy-27, gcy-33 and gcy-34 resulted in behavioral hypersensitivity to dilute (1 mM) quinine (p<0.01 for each). egl-4(gof) animals lacking ODR-1, GCY-27, GCY-33 or GCY-34 function showed diminished sensitivity to both (C) 10 mM quinine and (D) 1 mM quinine, similar to egl-4(gof) single mutant animals (p>0.1 for each double mutant when compared to egl-4(gof) animals). The percentage of animals responding is shown. (E) The osm-10 promoter [3] (ASH, ASI, PHA and PHB), srb-6 promoter [62] (ASH, ADL, ADF, PHA and PHB), and srbc-66 [62] (ASK) promoters were used in cell-selective rescue experiments. The quinine hypersensitivity of odr-1(lof) animals was rescued by srb-6p::odr-1 expression (p<0.001), but not osm-10p::odr-1 expression (p>0.5). gcy-27(lof) hypersensitivity was rescued by all three promoters (p<0.001 for each). Neither gcy-33(lof) nor gcy-34(lof) hypersensitivity was rescued using the osm-10 or srb-6 promoters (p>0.05 for each). The combined data of ≥3 independent lines, n≥120 transgenic animals, is shown. Error bars represent the standard error of the mean (SEM). Alleles used: egl-4(n479), odr-1(n1936), gcy-27(ok3653), gcy-33(ok232) and gcy-34(ok2953) loss-of-function and egl-4(ad450) gain-of-function. WT = the N2 wild-type strain. lof = loss-of-function. gof = gain-of-function.