Abstract
Salinity is a severe abiotic stress that affects plant growth and yield.Salinity stress activates jasmonate(JA)signaling in Arabidopsis thaliana,but the underlying molecular mechanism remains to be elucidated.In this study,we confirmed the activation of JA signaling under saline conditions and demonstrated the importance of the CORONATINE INSENS1TIVE1(COI1)-mediated JA signaling for this process.Phenotypic analyses reflected the negative regulation of JASMONATE ZIM-DOMAIN(JAZ)repressors during salinity stress-enhanced JA signaling.Mechanistic analyses revealed that JAZ proteins physically interact with ABSCISIC ACID-RESPONSIVE ELEMENT BINDING FACTOR1(ABF1),AREB1/ABF2,ABF3,and AREB2/ABF4,which belong to the basic leucine zipper(bZIP)transcription factor family and respond to salinity stress.Analyses on the ABF3 overexpression plants and ABF mutants indicated the positive role of ABF3 in regulating JA signaling under saline condition.Furthermore,ABF3 overexpression partially recovered the JA-related phenotypes of JAZ1-43A plants.Moreover,ABF3 was observed to indirectly activate ALLENE OXIDE SYNTHASE(AOS)transcription,but this activation was inhibited by JAZ1.In addition,ABF3 competitively bind to JAZ1,thereby decreasing the interaction between JAZ1 and MYC2,which is the master transcription factor controlling JA signaling.Collectively,our findings have clarified the regulatory effects of ABF3 on JA signaling and provide new insights into how JA signaling is enhanced following an exposure to salinity stress.
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