Fig. 3. Rescue of the behavioral defects associated with loss of fat-3 activity. (A) Exogenous AA and DHA, but not LIN, rescue the movement defects of fat-3(lg8101)/fat-3(qa1811) mutants. Animals were exposed to fatty acids from egg to adult. ^*P<0.0001 versus wild-type animals. (B) fat-3 expressed under the control of the neuronal promoter unc-119 (Exfat-3(+) neuron) but not under the control of the muscular promoter myo-3 (Exfat-3(+) muscle), completely rescues the egg-laying defect of fat-3(lg8101)/fat-3(qa1811) animals. Egl⁺ indicates hermaphrodites that were not consumed by embryos by the fourth day after reaching adulthood. (C) fat-3 expressed under the control of the neuronal promoter but not under the control of the muscular promoter or the intestinal promoter elt-2 (Exfat-3(+) intestine), almost completely rescues the movement defects of fat-3 (lg8101) homozygous animals. ^*P<0.0001 versus fat-3Exfat-3(+) animals. Data in A and C are plotted as mean ± s.e.m.