MAX3 deficiency recruits protective Pseudomonas via modulating the SL-ABA-flavonoid axis to suppress soil-borne pathogen infection
TL;DR
It is shown that MAX3 deficiency reshapes the Arabidopsis rhizosphere by altering ABA and flavonoid accumulation, which is associated with recruitment of beneficial Pseudomonas and enhanced resistance to bacterial wilt.
Abstract
Strigolactones (SLs) are carotenoid-derived hormones that regulate plant development and abiotic stress responses, but their role in regulating plant–microbe interactions remains unclear. Here, we show that Arabidopsis thaliana loss-of-function mutants of two SL biosynthetic genes, MORE AXILLARY GROWTH 3 (MAX3) and MAX4, exhibit opposite responses to soil-borne pathogen Ralstonia solanacearum, with max3 mutants displaying enhanced resistance, whereas max4 mutants are hypersusceptible. Exogenous SL analog rac-GR24 restores resistance in max4 mutants supporting a role for canonical SL-dependent immunity, while max3 mutants mediated resistance is SL-independent. Multi-omics analyses suggest that MAX3 deficiency is associated with enhanced abscisic acid (ABA) and flavonoid pathways under natural conditions, coinciding with the enrichment of beneficial Pseudomonas in rhizosphere. Both in vitro and in planta validations suggest that the ABA-flavonoid axis cooperatively enhances Pseudomonas-mediated niche competition and antibiotic biosynthesis, thereby potentially contributing to pathogen suppression. Our findings support a model in which MAX3 is associated with the modulation of rhizosphere-mediated defense, linking hormone signaling, secondary metabolism, and microbiome assembly in the context of soil-borne disease resistance. Here the authors show that MAX3 deficiency reshapes the Arabidopsis rhizosphere by altering ABA and flavonoid accumulation, which is associated with recruitment of beneficial Pseudomonas and enhanced resistance to bacterial wilt.