4.6 Article

Induction of systemic stress tolerance by brassinosteroid in Cucumis sativus

Journal

NEW PHYTOLOGIST
Volume 191, Issue 3, Pages 706-720

Publisher

WILEY
DOI: 10.1111/j.1469-8137.2011.03745.x

Keywords

brassinosteroid biosynthesis; phytohormones; reactive oxygen species; stress tolerance; systemic signal

Categories

Funding

  1. National Basic Research Program of China [2009CB119000]
  2. National Natural Science Foundation of China [31000905, 30671428, 30972033]
  3. Program for Promotion of Basic Research Activities for Innovative Bioscience (PROBRAIN)
  4. Foundation for the Author of National Excellent Doctoral Dissertation of China [200766]

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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.

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