The Physiological And Molecular Mechanism Of Root Development Response To H₂S In Arabidopsis Thaliana

Hydrogen sulfide（ H₂S） was identified as the third endogenous gaseous transmitter, following the discovery of nitric oxide（NO） and carbon monoxide（CO）,has been considered a key regulator of plant developmental processes and defenses. It has been reported Hydrogen sulfide（H₂S） is a gasotransmitter that modulates root system architecture（RSA） by affecting auxin distribution, however, the signaling transduction pathway underlying the process remain unclear. Here, we report that exogenous sodium hydrosulfide（NaHS）, a H2 S donor, reduced auxin accumulation and perception in Arabidopsis by triggering a signal transduction pathway including hydrogen peroxide（H2O2） accumulation, the activation of MPK6, and nitric oxide（NO） production; and thereby repressing primary root（PR） growth. Exogenous NaHS reduced auxin distribution by repressing auxin carriers expression and impeded auxin signaling by improving the stabilization of Aux/IAA transcriptional repressors in roots. NaHS induced a significant elevation in H2O2 and NO levels, two known signal molecules that modulated root growth. The ROS mutants rbohD, rbohF, rbohD/F,and the NOS mutant noa1 were insensitive to NaHS, suggested that both NO and ROS mediate the inhibitory effects of NaHS on PR growth. We provided evidence that NaHS-activated H2O2 production is required for NO generation. We found that MPK6 mediates the inductive effect of NaHS on NO production. Further study suggests that MPK6 functions in downstream of H2O2 and upstream of NO. Finally,we demonstrated that NaHS-activated of NO production was responsible for repressing auxin distribution and perception, reducing the meristematic cell division potential and stem cell niche activity in root tips. Together, our results suggest a signaling pathway in which NaHS induced H2O2 accumulation, thereby activatingMPK6, and then promotes NO production and subsequent repression of auxin signaling and meristem cell development, and finally resulted in PR growth inhibition.