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Induction of systemic stress tolerance by brassinosteroid in Cucumis sativus

Brassinosteroids (BRs) are a new class of plant hormones that are essential for plant growth and development. Here, the involvement of BRs in plant systemic tolerance to biotic and abiotic stresses was studied. The effects of 24-epibrassinolide (EBR) on plant stress tolerance were studied through th...

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Published in:The New phytologist 2011-08, Vol.191 (3), p.706-720
Main Authors: Xia, Xiao-Jian, Zhou, Yan-Hong, Ding, Ju, Shi, Kai, Asami, Tadao, Chen, Zhixiang, Yu, Jing-Quan
Format: Article
Language:English
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Summary:Brassinosteroids (BRs) are a new class of plant hormones that are essential for plant growth and development. Here, the involvement of BRs in plant systemic tolerance to biotic and abiotic stresses was studied. The effects of 24-epibrassinolide (EBR) on plant stress tolerance were studied through the assessment of symptoms of photooxidative stress by chlorophyll fluorescence imaging pulse amplitude modulation, the analysis of gene expression using quantitative real-time PCR and the measurement of hydrogen peroxide (H₂O₂) production using a spectrophotometric assay or confocal laser scanning microscopy. Treatment of primary leaves with EBR induced systemic tolerance to photooxidative stress in untreated upper and lower leaves. This was accompanied by the systemic accumulation of H₂O₂ and the systemic induction of genes associated with stress responses. Foliar treatment of EBR also enhanced root resistance to Fusarium wilt pathogen. Pharmacological study showed that EBR-induced systemic tolerance was dependent on local and systemic H₂O₂ accumulation. The expression of BR biosynthetic genes was repressed in EBR-treated leaves, but elevated significantly in untreated systemic leaves. Further analysis indicated that EBR-induced systemic induction of BR biosynthetic genes was mediated by systemically elevated H₂O₂. These results strongly argue that local EBR treatment can activate the continuous production of H₂O₂, and the autopropagative nature of the reactive oxygen species signal, in turn, mediates EBR-induced systemic tolerance.
ISSN:0028-646X
1469-8137
DOI:10.1111/j.1469-8137.2011.03745.x