Caffeine-induced food-avoidance behavior is mediated by neuroendocrine signals in Caenorhabditis elegans
Caffeine-induced food-avoidance behavior is mediated by neuroendocrine signals in Caenorhabditis elegans
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DOI：
10.5483/bmbrep.2017.50.1.126
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发表时间：
2017-01-01
期刊：
影响因子：
3.8
通讯作者：
Shim, Yhong-Hee
中科院分区：
文献类型：
--
作者：
Min, Hyemin;Youn, Esther;Shim, Yhong-Hee
高剂量的咖啡因摄入是一种发育应激源，并导致C. elegans，但其作用方式在很大程度上是未知的。在本研究中，我们探讨了咖啡因诱导的C。优雅的我们发现30 mM咖啡因诱导的厌恶表型是由JNK/MAPK通路、多巴胺能和多巴胺能神经内分泌信号介导的。在这个过程中，多巴胺能信号似乎是主要的途径，因为减少厌恶行为的cat-2突变体和JNK/MAPK途径基因的突变体显着恢复与多巴胺预处理。RNAi消减HSP-16.2（一种胞质伴侣蛋白）和CYP-35 A家族减少了厌恶表型，这在cat-2突变体中进一步减少，表明多巴胺能信号确实是咖啡因诱导的食物厌恶所需的主要信号。我们的研究结果表明，厌恶行为是蠕虫在高剂量咖啡因条件下生存的一种防御机制。
High-dose caffeine uptake is a developmental stressor and causes food-avoidance behavior (aversion phenotype) in C. elegans, but its mode of action is largely unknown. In this study, we investigated the molecular basis of the caffeine-induced aversion behavior in C. elegans. We found that aversion phenotype induced by 30 mM caffeine was mediated by JNK/MAPK pathway, serotonergic and dopaminergic neuroendocrine signals. In this process, the dopaminergic signaling appears to be the major pathway because the reduced aversion behavior in cat-2 mutants and mutants of JNK/MAPK pathway genes was significantly recovered by pretreatment with dopamine. RNAi depletion of hsp-16.2, a cytosolic chaperone, and cyp-35A family reduced the aversion phenotype, which was further reduced in cat-2 mutants, suggesting that dopaminergic signal is indeed dominantly required for the caffeine-induced food aversion. Our findings suggest that aversion behavior is a defense mechanism for worms to survive under the high-dose caffeine conditions.