4.4 Article

Ethylene, but not salicylic acid or methyl jasmonate, induces a resistance response against Phytophthora capsici in Habanero pepper

期刊

EUROPEAN JOURNAL OF PLANT PATHOLOGY
卷 131, 期 4, 页码 669-683

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SPRINGER
DOI: 10.1007/s10658-011-9841-z

关键词

Pathogenesis-related proteins; Phytohormones; Phytophthora blight

资金

  1. CONACYT [P48831, 208245, 56153]

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We sprayed defence-related plant growth regulators (salicylic acid, methyl jasmonate and ethephon) on one-month-old Habanero pepper seedlings cultivated in vitro. Twenty-four hours later, we inoculated the seedlings with a virulent strain of Phytophthora capsici and periodically evaluated the disease symptoms. At the concentrations used, neither salicylic acid nor methyl jasmonate generated a protective effect in the seedlings, which died less than 10 days post inoculation. However, the treatment with 5 mM ethephon delayed or prevented disease symptoms in 30% of the seedlings. Interestingly, blocking the ethylene receptor with a previous application of 300 mu M silver nitrate impeded the protective effects of ethephon. This result demonstrated that the plant resistance response required the perception of ethylene. Analysis of transcript populations in ethephon-treated seedlings revealed a direct correlation between survival and the accumulation of PR1, a gene marker of the systemic acquired resistance (SAR). Although the ethephon treatment also modified transcript levels of the plant defensin PDF1.2, a marker of the induced systemic resistance (ISR), in this case the accumulation also occurred when the ethylene receptor was blocked, suggesting a non-specific effect. The ethephon treatment did not modify the expression of NPR1 (a key transcriptional regulator of plant defence). Interestingly, transgenic pepper seedlings overexpressing endogenous PR10 or esterase genes, which are induced by the ET treatment, completely resisted the infection, which corroborated the importance of these genes in the defence response. Our results suggest that ethylene induced a systemic defence response in susceptible seedlings, possibly in an NPR1-independent pathway.

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