Rare earth (RE) ions at high concentrations are toxic to many organisms as they induce oxidative stress and cause improper incorporation of the ions into calcium-binding proteins. Although the mechanism… Click to show full abstract
Rare earth (RE) ions at high concentrations are toxic to many organisms as they induce oxidative stress and cause improper incorporation of the ions into calcium-binding proteins. Although the mechanism of action underlying the toxicity of REs has been identified, intracellular signaling pathways involved in stress responses against RE ions still remain unclear. In Caenorhabditis elegans, cellular responses against heavy metal stresses are primarily regulated by the c-Jun N-terminal kinase (JNK)-like mitogen-activated protein kinase (MAPK) pathway with a minor contribution of the p38-like MAPK pathway. In this study, we found that both JNK- and p38-like MAPK pathways were involved in stress responses against RE. Unlike heavy metal responses, mutations in both the JNK and p38 pathways caused similar hypersensitivity to RE ions. Although the signaling pathways used for these stress responses were found to be similar, the degree of their respective contribution slightly differed between heavy metal and RE ions.
               
Click one of the above tabs to view related content.