Hydrogen sulfide toxicity inhibits primary root growth through the ROS-NO pathway

High concentrations of hydrogen sulfide (H(2)S) are toxic to plants and inhibit their growth. Previous research indicated that high concentrations of H(2)S modulate the root system architecture (RSA) by affecting auxin transport; however, the signaling pathway underlying this process remains unclear. Here, we investigated the effects of exogenous sodium hydrosulfide (NaHS), an H(2)S donor, on primary root (PR) growth in Arabidopsis using pharmacological, physiological, and genetic approaches. H(2)S toxicity repressed PR growth by triggering a signal transduction pathway involving reactive oxygen species (ROS) accumulation, MITOGEN-ACTIVATED PROTEIN KINASE 6 (MPK6) activation, and nitric oxide (NO) production. Respiratory burst oxidase homolog mutants and an NO synthase mutant were less sensitive to NaHS, suggesting that both ROS and NO mediate the inhibitory effects of H(2)S on PR growth. We found that exogenous H(2)S-activated ROS production was required for NO generation and that MPK6 mediated H(2)S-induced NO production. MPK6 was shown to function downstream of ROS and upstream of NO. Finally, we demonstrated that exogenous H(2)S repressed the distribution of auxin and reduced the meristematic cell division potential in root tips, and NO was involved in this process.