title: Plant ERD2-like proteins function as endoplasmic reticulum luminal protein receptors and participate in programmed cell death during innate immunity.
abstract: The hypersensitive response (HR), a form of programmed cell death (PCD), is a tightly regulated innate immune response in plants that is hypothesized to restrict pathogen growth and disease development. Although considerable efforts have been made to understand HR PCD, it remains unknown whether the retrograde pathway from the Golgi to the endoplasmic reticulum (ER) is involved. Here we provide direct genetic evidence that two Nicotiana benthamiana homologs, ERD2a and ERD2b, function as ER luminal protein receptors and participate in HR PCD. Virus-induced gene silencing (VIGS) of ERD2a and/or ERD2b caused escape of ER-resident proteins from the ER, and resulted in plants that were more sensitive to ER stress. Silencing of ERD2b delayed HR PCD induced by the non-host pathogens Xanthomonas oryzae pv. oryzae and Pseudomonas syringae pv. tomato DC3000. However, both silencing of ERD2a and co-silencing of ERD2a and ERD2b exacerbated HR PCD. Individual and combined suppression of ERD2a and ERD2b exaggerated R gene-mediated cell death. Nevertheless, silencing of ERD2a and/or ERD2b had no detectable effects on bacterial growth. Furthermore, VIGS of several putative ligands of ERD2a/2b, including the ER quality control (ERQC) component genes BiP, CRT3 and UGGT, had different effects on HR PCD induced by different pathogens. This indicates that immunity-related cell death pathways are separate with respect to the genetic requirements for these ERQC components. These results suggest that ERD2a and ERD2b function as ER luminal protein receptors to ensure ERQC and alleviate ER stress, thus affecting HR PCD during the plant innate immune response.
authors.affiliation: MOE Key Laboratory of Bioinformatics, School of Life Sciences, Tsinghua University, Beijing 100084, China.
authors.forename: Guoyong
authors.initials: G
authors.lastname: Xu
authors.forename: Sizhun
authors.initials: S
authors.lastname: Li
authors.forename: Ke
authors.initials: K
authors.lastname: Xie
authors.forename: Qiang
authors.initials: Q
authors.lastname: Zhang
authors.forename: Yan
authors.initials: Y
authors.lastname: Wang
authors.forename: Yang
authors.initials: Y
authors.lastname: Tang
authors.forename: Dong
authors.initials: D
authors.lastname: Liu
authors.forename: Yiguo
authors.initials: Y
authors.lastname: Hong
authors.forename: Chenyang
authors.initials: C
authors.lastname: He
authors.forename: Yule
authors.initials: Y
authors.lastname: Liu
mesh_terms: D017209:Apoptosis / Q000235:genetics / Q000502:physiology*; D004721:Endoplasmic Reticulum / Q000378:metabolism*; D059865:Endoplasmic Reticulum Stress; D018506:Gene Expression Regulation, Plant; D020868:Gene Silencing; D005816:Genetic Complementation Test; D006056:Golgi Apparatus / Q000378:metabolism; D054884:Host-Pathogen Interactions; D010935:Plant Diseases / Q000276:immunology* / Q000382:microbiology; D057865:Plant Immunity; D018515:Plant Leaves / Q000235:genetics / Q000276:immunology / Q000382:microbiology / Q000502:physiology; D010940:Plant Proteins / Q000235:genetics / Q000378:metabolism*; D030821:Plants, Genetically Modified; D044224:Pseudomonas syringae / Q000502:physiology; D015398:Signal Transduction; D014026:Nicotiana / Q000235:genetics / Q000276:immunology / Q000382:microbiology / Q000502:physiology*; D014974:Xanthomonas / Q000502:physiology
chemical_list: D010940:Plant Proteins