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

Fig. 3.

Fig. 3

Caffeine-induced food-avoidance behavior was mediated by JNK/MAPK and neuroendocrine signaling. (A) Aversion phenotype in JNK/MAPK mutants (kgb-1, mlk-1, mek-1, jnk-1) after 0 mM or 30 mM caffeine treatment with or without acute-dopamine or serotonin treatment. 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 = 4099; kgb-1, n = 1559; mlk-1, n = 1638; mek-1, n = 1704; jnk-1, n = 929). Values are shown as average % food aversion ± s.d. (B) Aversion phenotype after RNAi depletion of cyp-35A2, cyp-35A4 in N2 and cat-2 mutants. After the RNAi depletion, the 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 (individual RNAi, n > 654). (C) Aversion phenotype after RNAi depletion of hsp-16.2 in N2 and cat-2 mutants. After the RNAi depletion, the 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 (individual RNAi, n > 723). Values are shown as average % food aversion. Error bars represent s.d. *P < 0.05. †P > 0.05.