An extragenic second-site mutation in the jar1-1 mutant suppresses the response to photoperiod stress independent of jasmonic acid.

Abstract

Extension of the light period causes photoperiod stress in Arabidopsis thaliana. The photoperiod stress phenotype is characterized by an induction of stress and cell death marker genes, the formation of reactive oxygen species (ROS) and enhanced formation of jasmonates during the night following the extended light period. Previously, experiments had shown that the jar1-1 mutant, carrying a point mutation in the jasmonoyl-isoleucine (JA-Ile) biosynthesis gene JAR1, showed a strongly reduced stress phenotype suggesting that JA-Ile is required for the stress response. Here, we have analyzed the roles of JA-Ile and JAR1 in more detail. While jar1-1 reduced the photoperiod stress phenotype indicating that JAR1 is required for the response to photoperiod stress, mutation of the ALLENE OXIDE SYNTHETASE (AOS) jasmonate biosynthesis gene did not rescue the stress phenotype. Further, analysis of jasmonate signaling mutants did not indicate their broad resistance to photoperiod stress. Unexpectedly, other JAR1 mutant alleles like jar1-11 and fin219-2 did not alleviate the photoperiod stress phenotype. Genetic analysis revealed that a recessive unlinked second-site mutation in the jar1-1 mutant background is responsible for the suppression of the photoperiod stress response. Taken together, these results suggest that JA-Ile is less important for the response to photoperiod stress than indicated by previous results.