Orchestration of hydrogen peroxide and nitric oxide in brassinosteroid-mediated systemic virus resistance inNicotiana benthamiana
Autor: | Xue-Ying Han, De-Hui Xi, Xing-Guang Deng, Da-Wei Zhang, Xue Zhou, Tong Zhu, Lijuan Zou, Hong-Hui Lin |
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Rok vydání: | 2016 |
Předmět: |
0106 biological sciences
0301 basic medicine Nicotiana benthamiana Plant Science Biology Nitric Oxide Models Biological 01 natural sciences Virus Nitric oxide 03 medical and health sciences chemistry.chemical_compound Gene Expression Regulation Plant Genes Reporter Brassinosteroids Tobacco Genetics Tobacco mosaic virus Gene silencing Brassinosteroid Disease Resistance Plant Diseases Plant Proteins NADPH oxidase NADPH Oxidases Hydrogen Peroxide Cell Biology biology.organism_classification Cell biology Plant Leaves Tobacco Mosaic Virus 030104 developmental biology chemistry Biochemistry biology.protein Signal transduction Reactive Oxygen Species Signal Transduction 010606 plant biology & botany |
Zdroj: | The Plant Journal. 85:478-493 |
ISSN: | 0960-7412 |
Popis: | Brassinosteroids (BRs) play essential roles in modulating plant growth, development and stress responses. Here, involvement of BRs in plant systemic resistance to virus was studied. Treatment of local leaves in Nicotiana benthamiana with BRs induced virus resistance in upper untreated leaves, accompanied by accumulations of H2O2 and NO. Scavenging of H2O2 or NO in upper leaves blocked BR-induced systemic virus resistance. BR-induced systemic H2O2 accumulation was blocked by local pharmacological inhibition of NADPH oxidase or silencing of respiratory burst oxidase homolog gene NbRBOHB, but not by systemic NADPH oxidase inhibition or NbRBOHA silencing. Silencing of the nitrite-dependent nitrate reductase gene NbNR or systemic pharmacological inhibition of NR compromised BR-triggered systemic NO accumulation, while local inhibition of NR, silencing of NbNOA1 and inhibition of NOS had little effect. Moreover, we provide evidence that BR-activated H2O2 is required for NO synthesis. Pharmacological scavenging or genetic inhibiting of H2O2 generation blocked BR-induced systemic NO production, but BR-induced H2O2 production was not sensitive to NO scavengers or silencing of NbNR. Systemically applied sodium nitroprusside rescued BR-induced systemic virus defense in NbRBOHB-silenced plants, but H2O2 did not reverse the effect of NbNR silencing on BR-induced systemic virus resistance. Finally, we demonstrate that the receptor kinase BRI1(BR insensitive 1) is an upstream component in BR-mediated systemic defense signaling, as silencing of NbBRI1 compromised the BR-induced H2O2 and NO production associated with systemic virus resistance. Together, our pharmacological and genetic data suggest the existence of a signaling pathway leading to BR-mediated systemic virus resistance that involves local Respiratory Burst Oxidase Homolog B (RBOHB)-dependent H2O2 production and subsequent systemic NR-dependent NO generation. |
Databáze: | OpenAIRE |
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