Brassinosteroids modulate the efficiency of plant immune responses to microbe-associated molecular patterns

被引:233
作者
Belkhadir, Youssef [2 ,3 ]
Jaillais, Yvon [2 ,3 ]
Epple, Petra [1 ]
Balsemao-Pires, Emilia [2 ,3 ]
Dangl, Jeffery L. [1 ,4 ]
Chory, Joanne [2 ,3 ]
机构
[1] Univ N Carolina, Dept Biol, Howard Hughes Med Inst, Chapel Hill, NC 27599 USA
[2] Salk Inst Biol Studies, Plant Biol Lab, La Jolla, CA 92037 USA
[3] Salk Inst Biol Studies, Howard Hughes Med Inst, La Jolla, CA 92037 USA
[4] Univ N Carolina, Carolina Ctr Genome Sci, Dept Microbiol & Immunol, Curriculum Genet, Chapel Hill, NC 27599 USA
基金
美国国家科学基金会; 美国国家卫生研究院;
关键词
brassinosteroid signaling; plant immune system signaling; signaling crosstalk; DISEASE RESISTANCE; BASAL DEFENSE; CELL-DEATH; ARABIDOPSIS; PHOSPHORYLATION; RECEPTORS; EFFECTORS; PATHWAYS; SYSTEM; BAK1;
D O I
10.1073/pnas.1112840108
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Metazoans and plants use pattern recognition receptors (PRRs) to sense conserved microbial-associated molecular patterns (MAMPs) in the extracellular environment. In plants, the bacterial MAMPs flagellin and elongation factor Tu (EF-Tu) activate distinct, phylogenetically related cell surface pattern recognition receptors of the leucine-rich repeat receptor kinase (LRR-RK) family called FLS2 and EF-Tu receptor, respectively. BAK1 is an LRR-RK coreceptor for both FLS2 and EF-Tu receptor. BAK1 is also a coreceptor for the plant brassinosteroid (BR) receptor, the LRR-RK BRI1. Binding of BR to BRI1 primarily promotes cell elongation. Here, we tune the BR pathway response to establish how plant cells can generate functionally different cellular outputs in response to MAMPs and pathogens. We demonstrate that BR can act antagonistically or synergistically with responses to MAMPs. We further show that the synergistic activities of BRs on MAMP responses require BAK1. Our results highlight the importance of plant steroid homeostasis as a critical step in the establishment of plant immunity. We propose that tradeoffs associated with plasticity in the face of infection are layered atop plant steroid developmental programs.
引用
收藏
页码:297 / 302
页数:6
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