Activation of defense response pathways by OGs and Flg22 elicitors in Arabidopsis seedlings

被引:388
作者
Denoux, Carine [1 ,2 ,3 ]
Galletti, Roberta [4 ]
Mammarella, Nicole [1 ,2 ]
Gopalan, Suresh [1 ,2 ]
Werck, Daniele [3 ]
De Lorenzo, Giulia [4 ]
Ferrari, Simone [4 ]
Ausubel, Frederick M. [1 ,2 ]
Dewdney, Julia [1 ,2 ]
机构
[1] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02114 USA
[2] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA
[3] Univ Strasbourg 1, CNRS, Inst Biol Mol Plantes, Strasbourg, France
[4] Univ Roma La Sapienza, Dipartimento Biol Vegetale, I-00185 Rome, Italy
基金
美国国家科学基金会; 美国国家卫生研究院;
关键词
D O I
10.1093/mp/ssn019
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
We carried out transcriptional profiling analysis in 10-d-old Arabidopsis thaliana seedlings treated with oligogalacturonides (OGs), oligosaccharides derived from the plant cell wall, or the bacterial flagellin peptide Flg22, general elicitors of the basal defense response in plants. Although detected by different receptors, both OGs and Flg22 trigger a fast and transient response that is both similar and comprehensive, and characterized by activation of early stages of multiple defense signaling pathways, particularly JA-associated processes. However, the response to Flg22 is stronger in both the number of genes differentially expressed and the amplitude of change. The magnitude of induction of individual genes is in both cases dose-dependent, but, even at very high concentrations, OGs do not induce a response that is as comprehensive as that seen with Flg22. While high doses of either microbe-associated molecular pattern (MAMP) elicit a late response that includes activation of senescence processes, SA-dependent secretory pathway genes and PR1 expression are substantially induced only by Flg22. These results suggest a lower threshold for activation of early responses than for sustained or SA-mediated late defenses. Expression patterns of amino-cyclopropane-carboxylate synthase genes also implicate ethylene biosynthesis in regulation of the late innate immune response.
引用
收藏
页码:423 / 445
页数:23
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