摘要
EFR is a plasma-membrane resident receptor responsible for recognition of microbial elongation factorTu （EF-Tu） and thus triggering plant innate immunity to fend off phytopathogens. Functional EFR must be subject to the endoplasmic reticulum quality control （ERQC） machinery for the correct folding and proper assembly in order to reach its final destination. Genetic studies have demonstrated that ERD2b, a counterpart of the yeast or mammalian HDEL receptor ERD2 for retaining proteins in the endoplasmic reticulum （ER） lumen, is required for EFR function in plants （Li et al., 2009）. In this study, we characterized the Arabidopsis glucosidase Ⅱ β--subunit via the H DEL motif against the non-redundant protein database. Data mining also revealed that the glucosidase Ⅱ β--subunit gene has a highly similar expression pattern to ERD2b and the other known ERQC components involved in EFR biogenesis. Importantly, the T-DNA insertion lines of the glucosidase Ⅱ β-subunit gene showed that EFR-controlled responses were substantially reduced or completely blocked in these mutants. The responses include seedling growth inhibition, induction of marker genes, MAP kinase activation, and callose deposition, trigged by peptide elf18, a full mimic of E F-Tu. Taken together, ourdata indicate a requirement of the glucosidase Ⅱ β-subunitfor EFR function.
EFR is a plasma-membrane resident receptor responsible for recognition of microbial elongation factorTu （EF-Tu） and thus triggering plant innate immunity to fend off phytopathogens. Functional EFR must be subject to the endoplasmic reticulum quality control （ERQC） machinery for the correct folding and proper assembly in order to reach its final destination. Genetic studies have demonstrated that ERD2b, a counterpart of the yeast or mammalian HDEL receptor ERD2 for retaining proteins in the endoplasmic reticulum （ER） lumen, is required for EFR function in plants （Li et al., 2009）. In this study, we characterized the Arabidopsis glucosidase Ⅱ β--subunit via the H DEL motif against the non-redundant protein database. Data mining also revealed that the glucosidase Ⅱ β--subunit gene has a highly similar expression pattern to ERD2b and the other known ERQC components involved in EFR biogenesis. Importantly, the T-DNA insertion lines of the glucosidase Ⅱ β-subunit gene showed that EFR-controlled responses were substantially reduced or completely blocked in these mutants. The responses include seedling growth inhibition, induction of marker genes, MAP kinase activation, and callose deposition, trigged by peptide elf18, a full mimic of E F-Tu. Taken together, ourdata indicate a requirement of the glucosidase Ⅱ β-subunitfor EFR function.
