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Signaling Pathway Underlying Hydrogen Sulfide Toxicity-mediated Root Growth Revealed

May 08, 2017     Email"> PrintText Size

Hydrogen sulfide (H2S) is a colorless gas with a characteristic odor of rotten eggs. Although low concentrations of H2S improve the tolerance of plants to abiotic and biotic stresses, high concentrations are toxic to plant growth. H2S toxicity-induced primary root (PR) growth inhibition has been reported; however, the signaling pathway underlying H2S toxicity-mediated root growth and development is still unclear. 

Prof. XU Jin and his team from Xishuangbanna Tropical Botanical Garden (XTBG) of the Chinese Academy of Sciences investigated the effects of exogenous sodium hydrosulfide (NaHS), an H2S donor, on primary root (PR) growth in Arabidopsis using pharmacological, physiological, and genetic approaches. 

The researchers analyzed the possible involvement of reactive oxygen species (ROS), nitric oxide (NO), and MITOGEN-ACTIVATED PROTEIN KINASE 6 (MPK6) in exogenous H2S-mediated PR growth. 

They found that H2S toxicity inhibited PR growth by reducing the meristematic cell division potential. ROS were involved in H2S toxicity-induced PR growth inhibition. NO was also required for the inhibition of PR growth by exogenous H2S. 

In addition to the auxin pathway, ROS and NO were also key players in the plant response to H2S toxicity. ROS production in roots induced by a high concentration of H2S inhibited PR growth, while ROS accumulation in roots activated MPK6.  

MPK6 then promoted NO production through both L-Arg- and NR-dependent routes. Elevated NO repressed the distribution of auxin in root tips, thereby reducing PR growth.  

The results indicated that H2S toxicity inhibited PR growth via both the ROS pathway and the auxin signaling pathway. The ROS-MPK6-NO signaling pathway mediated plant responses to H2S toxicity through morphological and physiological changes in the roots. 

The study entitled “Hydrogen sulfide toxicity inhibits primary root growth through the ROS-NO pathway” has been published in Scientific Reports.

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(Editor: ZHANG Nannan)

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