Integration of auxin/indole-3-acetic acid 17 and RGA-LIKE3 confers salt stress resistance through stabilization by nitric oxide in Arabidopsis.

Plants have developed complex mechanisms to respond to salt stress, depending on secondary messenger-mediated stress perception and signal transduction. Nitric oxide (NO) is widely known as a 'jack-of-all-trades' in stress responses. However, NO-mediated crosstalk between plant hormones remains unclear. In this study, we found that salt stabilized both AUXIN/INDOLE-3-ACETIC ACID 17 (Aux/IAA17) and RGA-LIKE3 (RGL3) proteins due to salt-induced NO production. Salt-induced NO overaccumulation and IAA17 overexpression decreased the transcripts of GA3ox genes, resulting in lower bioactive GA4. Further investigation showed that IAA17 directly interacted with RGL3 and increased its protein stability. Consistently, RGL3 stabilized IAA17 protein through inhibiting the interaction of TIR1 and IAA17 by competitively binding to IAA17. Moreover, both IAA17 and RGL3 conferred salt stress resistance. Overexpression of IAA17 and RGL3 partially alleviated the inhibitory effect of NO deficiency on salt resistance, whereas the iaa17 and rgl3 mutants displayed reduced responsiveness to NO-promoted salt resistance. Thus, the associations between IAA17 and gibberellin (GA) synthesis and signal transduction, and between the IAA17-interacting complex and the NO-mediated salt stress response were revealed based on physiological and genetic approaches. We conclude that integration of IAA17 and RGL3 is an essential component of NO-mediated salt stress response.