The MAX2‐KAI2 module promotes salicylic acid‐mediated immune responses in <i>Arabidopsis</i>

<jats:title>ABSTRACT</jats:title><jats:p><jats:italic>Arabidopsis</jats:italic> 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 <jats:italic>max2</jats:italic> mutation reduces resistance against <jats:italic>Pseudomonas syringae</jats:italic> pv. <jats:italic>tomato</jats:italic> (<jats:italic>Pst</jats:italic>). To uncover the mechanism of MAX2‐mediated resistance, we evaluated the resistance of various SL and KAR signaling pathway mutants. The resistance of SL‐deficient mutants and of <jats:italic>dwarf 14</jats:italic> (<jats:italic>d14</jats:italic>) was similar to that of the wild‐type, whereas the resistance of the <jats:italic>karrikin insensitive 2</jats:italic> (<jats:italic>kai2</jats:italic>) mutant was compromised, demonstrating that the KAR signaling pathway, not the SL signaling pathway, positively regulates the immune response. We measured the resistance of <jats:italic>smax1</jats:italic> and <jats:italic>smxl</jats:italic> mutants, as well as the double, triple, and quadruple mutants with <jats:italic>max2</jats:italic>, which revealed that both the <jats:italic>smax1</jats:italic> mutant and <jats:italic>smxl6/7/8</jats:italic> triple mutant rescue the low resistance phenotype of <jats:italic>max2</jats:italic> and that SMAX1 accumulation diminishes resistance. The susceptibility of <jats:italic>smax1D</jats:italic>, containing a degradation‐insensitive form of SMAX1, further confirmed the SMAX1 function in the resistance. The relationship between the accumulation 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 resistance against <jats:italic>Pst</jats:italic>, but KAR‐induced resistance depended 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.</jats:p>