期刊
PLANT PHYSIOLOGY
卷 164, 期 4, 页码 2184-2196出版社
AMER SOC PLANT BIOLOGISTS
DOI: 10.1104/pp.113.229369
关键词
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资金
- Natural Science Foundation of China [31270299, 31370301]
- Program for New Century Excellent Talents in Universities [NCET-11-0440]
- Natural Science Foundation of Hebei Province [C2012205005]
We previously reported that nitric oxide (NO) functions as a signal in thermotolerance. To illustrate its relationship with hydrogen peroxide (H2O2) in the tolerance of Arabidopsis (Arabidopsis thaliana) to heat shock (HS), we investigated the effects of heat on Arabidopsis seedlings of the following types: the wild type; three NADPH oxidase-defective mutants that exhibit reduced endogenous H2O2 levels (atrbohB, atrbohD, and atrbohB/ D); and a mutant that is resistant to inhibition by fosmidomycin (noa1, for nitric oxide-associated protein1). After HS, the NO levels in atrbohB, atrbohD, and atrbohB/ D seedlings were lower than that in wildtype seedlings. Treatment of the seedlings with sodium nitroprusside or S-nitroso-N-acetylpenicillamine partially rescued their heat sensitivity, suggesting that NO is involved in H2O2 signaling as a downstream factor. This point was verified by phenotypic analyses and thermotolerance testing of transgenic seedlings that overexpressed Nitrate reductase2 and NOA1, respectively, in an atrbohB/ D background. Electrophoretic mobility shift assays, western blotting, and real-time reverse transcription-polymerase chain reaction demonstrated that NO stimulated the DNA-binding activity of HS factors and the accumulation of HS proteins through H2O2. These data indicate that H2O2 acts upstream of NO in thermotolerance, which requires increased HS factor DNA-binding activity and HS protein accumulation.
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