Integration of Stress Signaling in Caenorhabditis elegans Through Cell-Nonautonomous Contributions of the JNK Homolog KGB-1.

摘要: Dealing with physiological stress is a necessity for all organisms, and the pathways charged this task are highly conserved in Metazoa . Accumulating evidence highlights cell-nonautonomous activation as an important mode of integrating responses at organism level. Work Caenorhabditis elegans highlighted importance such regulation unfolded protein response (UPR) gene expression downstream longevity-associated transcription factor DAF-16. Here we describe role JNK homolog KGB-1 these two modules. protects developing larvae from heavy metals folding (which found to be independent canonical UPR pathways), but sensitizes adults same stress, further shortening life span under normal conditions. This switch associated age-dependent antagonistic Using transgenic tissue-specific or examined contributions regulation, resistance, span. While cell-autonomous were observed, particularly epidermis, neuronal (and also muscle) effective driving intestinal induction, DAF-16, did not require target tissue. Additional genetic analyses revealed requirement UNC-13 mediating contributions, indicating involvement neurotransmission. Our results expand providing local cellular protection level whole organism.