4.5 Article

Small G protein RAC-2 regulates forgetting via the JNK-1 signalling pathway in Caenorhabditis elegans

期刊

EUROPEAN JOURNAL OF NEUROSCIENCE
卷 56, 期 12, 页码 6162-6173

出版社

WILEY
DOI: 10.1111/ejn.15855

关键词

Caenorhabditis elegans; forgetting; JNK-1; RAC-2; rho family G proteins; signalling pathway

资金

  1. National Natural Science Foundation Program of China
  2. [32170184]

向作者/读者索取更多资源

Recent research suggests that forgetting is an active biological process that removes outdated or irrelevant memories through the activation of specific genes and signal transduction pathways. This study reveals the involvement of RAC-2 and JNK-1 in the occurrence of forgetting in Caenorhabditis elegans, indicating their potential as a novel pathway.
Although forgetting was once regarded as a passive decline in memory and an occasional source of embarrassment, recent research suggests that it is an active biological process of removing outdated or irrelevant memories via activation of specific genes and signal transduction pathways. Rho family G proteins are known to have a role in synaptic plasticity mediated by the actin cytoskeleton. However, the current study reveals that another Rho guanosine triphosphate enzyme (GTPase), RAC-2, facilitates the occurrence of forgetting in Caenorhabditis elegans independent of actin dynamics. Functioning downstream of RAC-2 in the same signalling pathway, JNK-1 and its phosphorylated protein are required to positively regulate forgetting. The pan-neuronal rescue of RAC-2 or JNK-1, instead of AWC neuron-specific expression, reverses the delayed forgetting caused by the rac-2 mutation, which indicates that the involvement of RAC-2/JNK-1 in more than AWCs must be required. In summary, our work elucidates the action of the Rho GTPase RAC-2 and downstream JNK-1 as a potential novel pathway in forgetting in C. elegans.

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