Publication | Open Access
Specific ER quality control components required for biogenesis of the plant innate immune receptor EFR
273
Citations
43
References
2009
Year
Plant ImmunitySystems BiologySignal TransductionFunctional GenomicsDerived Peptides Elf18EngineeringPlant Defense GeneGeneticsImmunologyInnate ImmunityPattern Recognition ReceptorsPlant Innate ImmunityGene ExpressionMedicineCell BiologyPlant HormonePlant PhysiologyCrt3 Protein
Plant innate immunity relies on pattern‑recognition receptors such as EFR and FLS2 to detect PAMPs like EF‑Tu and flagellin. The study aimed to dissect the genetic basis of EFR‑mediated PTI in Arabidopsis. A forward‑genetic screen for elf18‑insensitive mutants uncovered alleles of CRT3, UGGT, and ERD2b, implicating ER quality‑control factors in EFR signaling. Loss of CRT3 abolishes EFR accumulation while ERD2b specifically retro‑translocates CRT3, demonstrating that distinct ER‑QC components are essential for PRR biogenesis without affecting FLS2.
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-recognition 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.
| Year | Citations | |
|---|---|---|
Page 1
Page 1