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. 2010 Dec;186(4):1309–1319. doi: 10.1534/genetics.110.119768

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Figure 2.— — ASER promotes salt avoidance and ASEL promotes salt attraction in daf-18 mutants. (A) NaCl chemotaxis of wild-type animals, daf-18(mg198null), age-1(hx546rf), akt-1(ok525null), daf-18(mg198); age-1(m333null), and daf-18(mg198); akt-1(ok525null) mutants under naive conditions. On the new assay format (see Figure S1B), daf-18(mg198) mutants show salt avoidance. Mutations of age-1 and akt-1 suppress the salt avoidance of the daf-18 mutants. (B) Effect of the dysfunction of ASE neurons due to the che-1(p674) mutation. The che-1(p674) mutation suppresses the salt avoidance of daf-18(mg198) mutants. (C) Chemotaxis of daf-18(mg198) mutants with 2-ASEL (otIs204[ceh-36p∷lsy-6]) or 2-ASER (lsy-6(ot71)). ASER promotes aversion and ASEL promotes attraction in daf-18 mutants. (D) A model deduced from the analysis of the role of ASER in daf-18 mutants. ASER promotes salt avoidance when the PI 3-kinase signaling is activated. Error bars represent SEM. (***) P < 0.001, (*) P < 0.05, Bonferroni t-test. n.s., not significant.