Journal
SCIENCE
Volume 343, Issue 6178, Pages 1509-1512Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1248849
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Funding
- United Kingdom Biotechnology and Biological Sciences Research Council
- U.S. Department of Energy (the Chemical Sciences, Geosciences, and Biosciences Division, Office of Basic Energy Sciences, Office of Science) [DE-FG02-91ER20021]
- U.S. National Institutes of Health [R01AI060761]
- Gordon and Betty Moore Foundation [GBMF3037]
- National Science Foundation [MCB-0742411, 0740211]
- USDA-ARS
- Federation of European Biochemical Societies (FEBS)
- KAKENHI [23580068]
- Excellent Young Researcher Overseas Visit Program
- Uehara memorial foundation
- European Molecular Biology Organization
- Fundacion Ramon Areces
- Biotechnology and Biological Sciences Research Council [BB/E017134/1, BB/G024944/1] Funding Source: researchfish
- Directorate For Engineering [0740211] Funding Source: National Science Foundation
- Div Of Industrial Innovation & Partnersh [0740211] Funding Source: National Science Foundation
- Grants-in-Aid for Scientific Research [23580068] Funding Source: KAKEN
- BBSRC [BB/G024944/1, BB/E017134/1] Funding Source: UKRI
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Innate immunity relies on the perception of pathogen-associated molecular patterns (PAMPs) by pattern-recognition receptors (PRRs) located on the host cell's surface. Many plant PRRs are kinases. Here, we report that the Arabidopsis receptor kinase EF-TU RECEPTOR (EFR), which perceives the elf18 peptide derived from bacterial elongation factor Tu, is activated upon ligand binding by phosphorylation on its tyrosine residues. Phosphorylation of a single tyrosine residue, Y836, is required for activation of EFR and downstream immunity to the phytopathogenic bacterium Pseudomonas syringae. A tyrosine phosphatase, HopAO1, secreted by P. syringae, reduces EFR phosphorylation and prevents subsequent immune responses. Thus, host and pathogen compete to take control of PRR tyrosine phosphorylation used to initiate antibacterial immunity.
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