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. 2013 Jun;29(2):182–192. doi: 10.5423/PPJ.SI.11.2012.0173.R2

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© The Korean Society of Plant Pathology

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Fig. 7 — Working model of the modulation of S. marcescens 90–166-elicited induced systemic resistance (ISR) in acyl-homoserine lactone-producing (AHL) or -degrading (AiiA) tobacco plants. In AHL plants, AHL produced by tobacco induces 2,3-butanediol synthesis after binding to the budB (luxR homologue) product. The 2,3-butanediol elicits jasmonic acid (JA)-dependent plant systemic defense. The JA defense mechanism in tobacco confers systemic resistance to P. carotovorum. Based on salicylic acid (SA) and JA antagonism, induction of JA signaling may suppress SA signaling leading to a reduction in ISR to CMV.