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PLoS One. 2012;7(11):e49800. doi: 10.1371/journal.pone.0049800. Epub 2012 Nov 21.

H(2) enhances arabidopsis salt tolerance by manipulating ZAT10/12-mediated antioxidant defence and controlling sodium exclusion.

Author information

1
College of Life Sciences, Co. Laboratory of Nanjing Agricultural University, Nanjing, Jiangsu Province, China.

Abstract

BACKGROUND:

The metabolism of hydrogen gas (H(2)) in bacteria and algae has been extensively studied for the interesting of developing H(2)-based fuel. Recently, H(2) is recognized as a therapeutic antioxidant and activates several signalling pathways in clinical trials. However, underlying physiological roles and mechanisms of H(2) in plants as well as its signalling cascade remain unknown.

METHODOLOGY/PRINCIPAL FINDINGS:

In this report, histochemical, molecular, immunological and genetic approaches were applied to characterize the participation of H(2) in enhancing Arabidopsis salt tolerance. An increase of endogenous H(2) release was observed 6 hr after exposure to 150 mM NaCl. Arabidopsis pretreated with 50% H(2)-saturated liquid medium, mimicking the induction of endogenous H(2) release when subsequently exposed to NaCl, effectively decreased salinity-induced growth inhibition. Further results showed that H(2) pretreatment modulated genes/proteins of zinc-finger transcription factor ZAT10/12 and related antioxidant defence enzymes, thus significantly counteracting the NaCl-induced reactive oxygen species (ROS) overproduction and lipid peroxidation. Additionally, H(2) pretreatment maintained ion homeostasis by regulating the antiporters and H(+) pump responsible for Na(+) exclusion (in particular) and compartmentation. Genetic evidence suggested that SOS1 and cAPX1 might be the target genes of H(2) signalling.

CONCLUSIONS:

Overall, our findings indicate that H(2) acts as a novel and cytoprotective regulator in coupling ZAT10/12-mediated antioxidant defence and maintenance of ion homeostasis in the improvement of Arabidopsis salt tolerance.

PMID:
23185443
PMCID:
PMC3504229
DOI:
10.1371/journal.pone.0049800
[Indexed for MEDLINE]
Free PMC Article

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