Sulfonamides Inhibit Root Growth via ROS-Triggered and MPK3/6-Modulated Synthesis of the Ethylene Precursor ACC.

Sulfonamide antibiotics threaten ecosystems, yet their phytotoxic mechanisms remain elusive. Here, we demonstrate that sulfonamides inhibit root growth by disrupting the ROS-ethylene signaling axis. Sulfadiazine (SD) strongly inhibits root elongation, an effect strictly dependent on ACS1, as the acs1-1 mutant is completely insensitive. Mechanistically, SD triggers an RBOH-dependent ROS burst that transcriptionally induces ACS1. Since ACS1 forms active heterodimers with ACS2/ACS6, acs2-1 and acs6-1 mutants exhibit partial insensitivity. Furthermore, SD partially depends on the MPK3/6 cascade to post-translationally stabilize ACS2/ACS6, with mpk3 and mpk6 mutants showing partial resistance. Collectively, sulfonamides employ a dual-pronged mechanism: ROS transcriptionally activate ACS1, while MPK3/6 post-translationally stabilizes ACS2/ACS6, driving aberrant ethylene precursor ACC biosynthesis and root growth inhibition.