期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 106, 期 37, 页码 15973-15978出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0905532106
关键词
endoplasmic reticulum; innate immunity; receptor kinase
资金
- ERA-NET Plant Genomics
- Gatsby Foundation
- Biotechnology and Biological Sciences Research Council [BB/F021046/1]
- EMBO Long-Term Fellowship
- Swiss National Foundation [31003A-120655]
- Biotechnology and Biological Sciences Research Council [BB/E024874/1, BB/F021046/1] Funding Source: researchfish
- Swiss National Science Foundation (SNF) [31003A-120655] Funding Source: Swiss National Science Foundation (SNF)
- BBSRC [BB/F021046/1, BB/E024874/1] Funding Source: UKRI
Plant innate immunity depends in part on recognition of pathogen-associated molecular patterns (PAMPs), such as bacterial flagellin, EF-Tu, and fungal chitin. Recognition is mediated by pattern-recogntition receptors (PRRs) and results in PAMP-triggered immunity. EF-Tu and flagellin, and the derived peptides elf18 and flg22, are recognized in Arabidopsis by the leucine-rich repeat receptor kinases (LRR-RK), EFR and FLS2, respectively. To gain insights into the molecular mechanisms underlying PTI, we investigated EFR-mediated PTI using genetics. A forward-genetic screen for Arabidopsis elf18-insensitive (elfin) mutants revealed multiple alleles of calreticulin3 (CRT3), UDP-glucose glycoprotein glucosyl transferase (UGGT), and an HDEL receptor family member (ERD2b), potentially involved in endoplasmic reticulum quality control (ER-QC). Strikingly, FLS2-mediated responses were not impaired in crt3, uggt, and erd2b null mutants, revealing that the identified mutations are specific to EFR. A crt3 null mutant did not accumulate EFR protein, suggesting that EFR is a substrate for CRT3. Interestingly, Erd2b did not accumulate CRT3 protein, although they accumulate wild-type levels of other ER proteins. ERD2B seems therefore to be a specific HDEL receptor for CRT3 that allows its retro-translocation from the Golgi to the ER. These data reveal a previously unsuspected role of a specific subset of ER-QC machinery components for PRR accumulation in plant innate immunity.
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