Fig 7. TORC2/PKC-2 pathway functions in neurons, whereas TORC2/SGK-1 pathway functions in the intestine. (A) Neuronal (
unc-14 promoter)and intestinal (
ges-1 promoter) expression of
sinh-1 cDNA rescued the chemotaxis defects of the
sinh-1(
pe420) mutant after low-salt/food(-) conditioning.(B) Pan-neuronal expression (H20 promoter) and ASER-specific expression (
gcy-5 promoter), but not intestine-specific expression (
ges-1 promoter), ofthe
pkc-2 cDNA rescued the chemotaxis abnormality of the
pkc-2(
ok328) mutant after low-salt/food(-) conditioning. (C) Intestine-specific expression (
sgk1B promoter or
ges-1 promoter), but not pan-neuronal expression (H20 promoter), of
sgk-1 isoform B was sufficient for rescuing the chemotaxis defect ofthe
sgk-1(
ok538) mutant after low-salt/food (-) conditioning. (D) Intestine-specific expression of the active form of
sgk-1 suppressed the chemotaxis defectof the
sinh-1(
pe420) mutant after low-salt/food(-) conditioning. Error bars, s.e.m.; *p < 0.05, **p < 0.01, n.s. = not significant (Dunnett's test, N=9).