4.7 Article

Analysis of defensive responses activated by volatile allo-ocimene treatment in Arabidopsis thaliana

Journal

PHYTOCHEMISTRY
Volume 67, Issue 14, Pages 1520-1529

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.phytochem.2006.05.027

Keywords

Arabidopsis thaliana; Cruciferae; defensive response; Botrytis cinerea; camalexin; lignification; allo-ocimene

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Since volatile allo-ocimene enhances resistance of Arabidopsis thaliana against Botrytis cinerea, we attempted to dissect the factors involved in this induced resistance. The penetration of B. cinerea hyphae into Arabidopsis epidermis and the growth of hyphae after penetration were suppressed on allo-ocimene-treated leaves. allo-Ocimene also induced lignification on cell walls and veins of the leaves. The treatment induced accumulation of antifungal substances including the Arabidopsis phytoalexin, camalexin. Induction of lignification and accumulation of camalexin elicited by R cinerea infection on Arabidopsis leaves after treating with allo-ocimene was faster and more intense than that observed with the leaves that had not been treated with this volatile. This suggested that allo-ocimene could prime defensive responses in Arabidopsis. allo-Ocimene enhanced resistant against B. cinerea in an ethylene resistant mutant (etr1-1), a jasmonic acid resistant mutant (jar1-1) and a salicylic acid resistant mutant (npr1-1). Thus, it is suggested that a signaling pathway independent for ETR1, JAR1 and NPR1 was operative to induce the resistance. The series of responses observed after allo-ocimene-treatment was mostly similar to that observed after C6-aldehyde-treatment. The effect of C6-aldehyde-treatment has been largely accounted to the chemical reactivities of the compounds; however, from this result it can be suggested that resistance responses of Arabidopsis could be induced by the volatiles mostly independent on their reactivities and that a common signaling pathway unaffected by the reactivities of compound was activated by the volatiles. (c) 2006 Elsevier Ltd. All rights reserved.

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