期刊
PLANT PHYSIOLOGY
卷 162, 期 2, 页码 1018-1029出版社
AMER SOC PLANT BIOLOGISTS
DOI: 10.1104/pp.113.219659
关键词
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资金
- Texas A&M University startup funds
- National Institutes of Health [RO1GM092772, R01GM092893]
- National Science Foundation [MCB-1054298, IOS-1030250]
- US Department of Agriculture National Institute of Food and Agriculture [2010-65108-20527]
- China Scholarship Council
- 973 program of the Ministry of Science and Technology of China [2011CB100700]
- Direct For Biological Sciences
- Division Of Integrative Organismal Systems [1030302] Funding Source: National Science Foundation
- Direct For Biological Sciences
- Div Of Molecular and Cellular Bioscience [1054298] Funding Source: National Science Foundation
To accomplish successful infection, pathogens deploy complex strategies to interfere with host defense systems and subvert host physiology to favor pathogen survival and multiplication. Modulation of plant auxin physiology and signaling is emerging as a common virulence strategy for phytobacteria to cause diseases. However, the underlying mechanisms remain largely elusive. We have previously shown that the Pseudomonas syringae type III effector AvrRpt2 alters Arabidopsis (Arabidopsis thaliana) auxin physiology. Here, we report that AvrRpt2 promotes auxin response by stimulating the turnover of auxin/indole acetic acid (Aux/IAA) proteins, the key negative regulators in auxin signaling. AvrRpt2 acts additively with auxin to stimulate Aux/IAA turnover, suggesting distinct, yet proteasome-dependent, mechanisms operated by AvrRpt2 and auxin to control Aux/IAA stability. Cysteine protease activity is required for AvrRpt2-stimulated auxin signaling and Aux/IAA degradation. Importantly, transgenic plants expressing the dominant axr2-1 mutation recalcitrant to AvrRpt2-mediated degradation ameliorated the virulence functions of AvrRpt2 but did not alter the avirulent function mediated by the corresponding RPS2 resistance protein. Thus, promoting auxin response via modulating the stability of the key transcription repressors Aux/IAA is a mechanism used by the bacterial type III effector AvrRpt2 to promote pathogenicity.
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