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. 2017 Jan 31;50(1):31–36. doi: 10.5483/BMBRep.2017.50.1.126

Fig. 2.

Fig. 2

The JNK/MAPK pathway and neuronal signaling were required for caffeine-induced aversion phenotype. (A) The JNK/MAPK pathway mediates caffeine-induced aversion phenotype demonstrated by RNAi depletion of tir-1, sek-1, pmk-1, mlk-1, mek-1, vhp-1, kgb-1, jkk-1 and jnk-1 in N2 worms. After RNAi depletion, synchronized L1 larvae were cultured on NGM agar plates containing 0 or 30 mM caffeine, and the aversion phenotype was observed at 24 h after caffeine treatment (mock RNAi, n = 894; tir-1 RNAi, n = 821; sek-1 RNAi, n = 797; pmk-1 RNAi, n = 877; mlk-1 RNAi, n = 676; mek-1 RNAi, n = 874; vhp-1 RNAi, n = 809; kgb-1 RNAi, n = 781; jkk-1 RNAi, n = 1020; jnk-1 RNAi, n = 898). (B) Dopamine-deficient cat-2, serotonin-deficient tph-1, serotonin and dopamine-deficient bas-1 mutants showed defects in food aversion at 30 mM caffeine. cat-2, tph-1 and bas-1 mutant worms synchronized at the L1 larval stage were cultured on NGM agar plates containing 0 or 30 mM caffeine, and the aversion phenotype was observed at 24 h after the caffeine treatment (N2, n = 589; cat-2, n = 380; tph-1, n = 966; bas-1, n = 623). (C, D) N2, cat-2, tph-1 and bas-1 worms synchronized at the L1 larval stage were pre-treated for 10 min with dopamine (DA) or serotonin (5-HT), cultured on NGM agar plates containing 0 or 30 mM caffeine, and the aversion phenotype was monitored at 24 h after caffeine treatment (N2, n = 793; cat-2, n = 511; tph-1, n = 763; bas-1, n = 524). Values are shown as average % food aversion. Error bars represent s.d. *P < 0.05. **P < 0.005. †P > 0.05.