Abstract
High concentrations of hydrogen sulfide (H2S) are toxic to plants and inhibit their growth. Previous research indicated that high concentrations of H2S 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 H2S donor, on primary root (PR) growth in Arabidopsis using pharmacological, physiological, and genetic approaches. H2S 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 H2S on PR growth. We found that exogenous H2S-activated ROS production was required for NO generation and that MPK6 mediated H2S-induced NO production. MPK6 was shown to function downstream of ROS and upstream of NO. Finally, we demonstrated that exogenous H2S repressed the distribution of auxin and reduced the meristematic cell division potential in root tips, and NO was involved in this process.
Highlights
Hydrogen sulfide (H2S) is a colorless gas with a characteristic odor of rotten eggs
We showed that the activation of MITOGEN-ACTIVATED PROTEIN KINASE 6 (MPK6), NADPH oxidase-dependent H2O2 synthesis, Nia1/NOA1-dependent nitric oxide (NO) production, and the regulation of auxin perception are all required for the inhibition of primary root (PR) growth by exogenous H2S
We found that exogenous H2S-induced NO production is mediated by reactive oxygen species (ROS) and that the modulation of NO production by ROS required the activation of MPK6
Summary
Hydrogen sulfide (H2S) is a colorless gas with a characteristic odor of rotten eggs. Low concentrations of H2S improve the tolerance of plants to pathogens[1], osmotic stress, salt stress, heat shock, and heavy metal stresses[2,3,4,5,6]. H2S toxicity-induced primary root (PR) growth inhibition has been reported[11]; the signaling pathway underlying H2S toxicity-mediated root growth and development is still unclear. H2S acts upstream of indole3-acetic acid (IAA) and NO to regulate root growth and development[9]; the signaling modulation mechanisms involved are largely unclear. Mitogen-activated protein kinase (MAPK) cascades, which consist of MAPKKK (MEKK), MAPKK (MKK), and MAPK (MPK), are highly conserved signaling transduction pathways found in animals, plants and microbes[19, 20]. Root growth and development are largely influenced by plant hormones, especially auxin[27]. Jia et al.[11] showed that high levels of H2S inhibit auxin transport and result in alterations in root system development by modulating the polar subcellular distribution of PIN proteins[11]
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