Jasmonate complements the function of Arabidopsis lipoxygenase3 in salinity stress response.

The functions of jasmonic acid (JA) in various stress responses have been uncovered in details, but its role in salt tolerance remains unclear. Here, we characterize the function of Arabidopsis lipoxygenase3 (LOX3), an enzyme involved in JA synthesis, in salt stress response. The transcriptional analysis indicated that LOX3 was dramatically induced under salt treatment. Compared with wild type, the lox3 mutant exhibited hypersensitivity to salt stress in germination and different developmental stages. Interestingly, methyl jasmonate (MeJA) rescued the salt sensitivity phenotypes of the lox3 mutant, suggesting the impairment of salinity response in the mutant may be mediated by JA. Furthermore, the lateral root number of the lox3 mutant was similar with that in wild type under normal condition, but less than that in wild type during salt treatment, and this lateral root sensitivity phenotype was also complemented by exogenous MeJA. In addition, the measurement of oxylipins in the lox3 mutant and the analysis on germination of the JA receptor coi1 mutant under salt stress supported that JA may regulate the early response to salinity. In conclusion, we characterized the novel function of LOX3 in salinity stress response, and found that the salt hypersensitivity of the lox3 mutant can be complemented by MeJA, providing new evidence for the association between JA and salt tolerance.