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

Figure 1. C. elegans EGL-4 regulates quinine sensitivity in ASH.

Figure 1

(A) egl-4(lof) animals respond better than wild-type animals to dilute (1 mM) quinine, while egl-4(gof) animals show a decreased sensitivity to 10 mM quinine, when compared to wild-type animals. p<0.0001 for each. (B) The ASH sensory neurons are the primary neurons used to detect quinine, but the ASK neurons also contribute [7]. The osm-10 [3], srb-6 [61] and srbc-66 [62] promoters were used to drive expression of wild-type egl-4 in egl-4(lof) animals. The osm-10 promoter expresses in ASH, ASI, PHA and PHB, while the srb-6 promoter drives expression in ASH, ADL, ADF, PHA and PHB. ASH is the only head sensory neuron common to both promoters. The srbc-66 promoter expresses in ASK. While egl-4(lof) animals respond better than wild-type animals to 1 mM quinine, restoring EGL-4 function in ASH significantly diminished this hypersensitivity (p<0.0001 for both). EGL-4 expression in ASK had no effect (p>0.5). (C) RNAi knock-down of egl-4 in the ASH sensory neurons of otherwise wild-type animals, using the osm-10 [3] or srb-6 [61] promoter resulted in behavioral hypersensitivity to dilute (1 mM) quinine, similar to egl-4(lof) animals (p<0.0001 when compared to N2 animals for both transgenes). The percentage of animals responding is shown. 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) loss-of-function and egl-4(ad450) gain-of-function. WT = the N2 wild-type strain. lof = loss-of-function. gof = gain-of-function.