Signal crosstalk between nitric oxide and hydrogen sulfide may be involved in hydrogen peroxide-induced thermotolerance in maize seedlings

Signal crosstalk between nitric oxide and hydrogen sulfide may be involved in hydrogen... Hydrogen peroxide (H2O2) and nitric oxide (NO) function as signal molecules in plant cells. Recently, hydrogen sulfide (H2S) has been found to have similar functions, but their interactions in the acquisition of thermotolerance in plants remain elusive. In current work, pretreatment with H2O2 rapidly induced endogenous H2O2 accumulation, which in turn improved survival percentage of maize seedlings (Zea mays L.) under heat stress, but these effects were eliminated by H2O2 scavenger dimethylthiourea indicating that H2O2-induced thermotolerance was involved in the accumulation of endogenous H2O2. H2O2 pretreatment also increased endogenous NO content, but this increase was abolished by NO scavenger cPTIO. Exogenously applied H2O2 also stimulated increase in the activity of L-cystine desulfhydrase, a key enzyme in H2S biosyn-thesis, followed by inducing endogenous H2S accumulation, while this accumulation was diminished by cPTIO. In addition, H2O2-induced thermotolerance was enhanced by NO donor sodium nitroprusside and H2S donors NaHS as well as GYY4137, respectively, and weakened by cPTIO, DL-propargylglycine (inhibitor of H2S biosynthesis) and hypotaurine (H2S scavenger). All of the above-mentioned results showed that H2O2 treatment could improve thermotolerance in maize seedlings, and the acquisition of thermotolerance induced by H2O2 may be involved in downstream signal crosstalk between NO and H2S. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Russian Journal of Plant Physiology Springer Journals

Signal crosstalk between nitric oxide and hydrogen sulfide may be involved in hydrogen peroxide-induced thermotolerance in maize seedlings

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Publisher
Pleiades Publishing
Copyright
Copyright © 2015 by Pleiades Publishing, Ltd.
Subject
Life Sciences; Plant Physiology; Plant Sciences
ISSN
1021-4437
eISSN
1608-3407
D.O.I.
10.1134/S1021443715030127
Publisher site
See Article on Publisher Site

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