Induced defence in tobacco by Pseudomonas chlororaphis strain O6 involves at least the ethylene pathway

被引:79
作者
Spencer, M
Ryu, CM
Yang, KY
Kim, YC
Kloepper, JW
Anderson, AJ
机构
[1] Utah State Univ, Dept Biol, Logan, UT 84322 USA
[2] Chonnam Natl Univ, Coll Agr & Life Sci, Agr Plant Stress Res Ctr, Gwangju 500757, South Korea
[3] Chonnam Natl Univ, Coll Agr & Life Sci, Appl Plant Sci Div, Gwangju 500757, South Korea
[4] Auburn Univ, Dept Entomol & Plant Pathol, Auburn, AL 36849 USA
关键词
Erwinia carotovora subsp carotovora; ethylene; GacS; induced resistance; phenazines; plant defense signaling; Pseudomonas chlororaphis O6; Pseudomonas syringae pv. tabaci;
D O I
10.1016/j.pmpp.2003.09.002
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
The antifungal phenazines produced by certain root colonizing pseudomonads are credited with contributing to the biocontrol activity of these isolates. However, the phenazine producer Pseudomonas chlororaphis O6 also induces systemic resistance in tobacco. Protection against two foliar bacterial pathogens, the wild fire pathogen, Pseudomonas syringae pv. tabaci, and Erwinia carotovora subsp. carotovora that causes a soft rot, was observed. A mutation in the bacterial global regulator gacS gene eliminated certain secondary traits, including phenazine production, but did not prevent induction of resistance in tobacco to P. syringae pv. tabaci. However, induction of resistance to E. carotovora subsp. carotovora was impaired in plants colonized by the GacS mutant compared to the level of protection in plants colonized by wild-type P. chlororaphis O6. Colonization by both the wild-type and the GacS mutant caused increased accumulation for transcripts of plant defense genes regulated by ethylene. Tobacco transformed with a mutant etr1 gene to reduce ethylene sensitivity did not display induced resistance to E. carotovora when colonized by P. chlororaphis O6. We conclude that inducers other than phenazines appear to initiate the pathways for systemic resistance induced by P. chlororaphis O6. (C) 2003 Elsevier Ltd. All rights reserved.
引用
收藏
页码:27 / 34
页数:8
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