The MAX2-KAI2 Module Promotes Salicylic Acid-Mediated Immune Responses in Arabidopsis

Arabidopsis MORE AXILLARY GROWTH2(MAX2)is a key component in the strigolactone(SL)and karrikin(KAR)signaling pathways and regulates the degradation of SUPPRESSOR OF MAX2 1/SMAX1-like(SMAX1/SMXL)proteins,which are transcriptional co-repressors that regulate plant architecture,as well as abiotic and biotic stress responses.The max2 mutation reduces resistance against Pseudomonas syringae pv.tomato(Pst).To uncover the mechanism of MAX2-mediated resistance,we evaluated the resistance of various SL and KAR signaling pathway mutants.The re-sistance of SL-deficient mutants and of dwarf 14(d14)was similar to that of the wild-type,whereas the resistance of the karrikin insensitive 2(kai2)mutant was compromised,demonstrating that the KAR signaling pathway,not the SL signaling pathway,positively regulates the immune re-sponse.We measured the resistance of smax1 and smxl mutants,as well as the double,triple,and quadruple mutants with max2,which revealed that both the smax1 mutant and smxl6/7/8 triple mutant rescue the low resistance phenotype of max2 and that SMAX1 accumulation diminishes resistance.The susceptibility of smax1D,con-taining a degradation-insensitive form of SMAX1,further confirmed the SMAX1 function in the re-sistance.The relationship between the accumu-lation of SMAX1/SMXLs and disease resistance suggested that the inhibitory activity of SMAX1 to resistance requires SMXL6/7/8.Moreover,the exogenous application of KAR2 enhanced resist-ance against Pst,but KAR-induced resistance de-pended on salicylic acid(SA)signaling.Inhibition of karrikin signaling delayed SA-mediated defense responses and inhibited pathogen-induced protein biosynthesis.Together,we propose that the MAX2-KAI2-SMAX1 complex regulates resistance with the assistance of SMXL6/7/8 and SA signaling and that SMAX1/SMXLs possibly form a multimeric complex with their target transcription factors to fine tune immune responses.