Retromer Contributes to Immunity-Associated Cell Death in Arabidopsis

• Published in: The Plant cell Vol. 27; no. 2; pp. 463 - 479
• Main Authors: Munch, David, Teh, Ooi-Kock, Malinovsky, Frederikke Gro, Liu, Qinsong, Vetukuri, Ramesh R., Kasmi, Farid El, Brodersen, Peter, Hara-Nishimura, Ikuko, Dangl, Jeffery L., Petersen, Morten, Mundy, John, Hofius, Daniel
• Format: Journal Article
• Language: English
• Published: United States American Society of Plant Biologists 01.02.2015
• Subjects: Agricultural Science; Apoptosis; Arabidopsis; Arabidopsis - cytology; Arabidopsis - genetics; Arabidopsis - immunology; Arabidopsis Proteins - metabolism; Arabidopsis thaliana; Autophagy; Cell death; Disease resistance; Disease Resistance - immunology; Endocytosis; Genes, Plant; Green Fluorescent Proteins - metabolism; Jordbruksvetenskap; Multiprotein Complexes - metabolism; Multivesicular Bodies - metabolism; Mutation; Pathogens; Phenotypes; Plant cells; Plant Diseases - immunology; Plant Immunity; Plants; Protein Binding; Protein Subunits - metabolism; Protein Transport; Receptors; Seedlings; Sequence Homology, Amino Acid; Yeasts
• ISSN: 1040-4651; 1532-298X; 1532-298X
• DOI: 10.1105/tpc.114.132043

Membrane trafficking is required during plant immune responses, but its contribution to the hypersensitive response (HR), a form of programmed cell death (PCD) associated with effector-triggered immunity, is not well understood. HR is induced by nucleotide binding-leucine-rich repeat (NB-LRR) immune receptors and can involve vacuole-mediated processes, including autophagy. We previously isolated lazarus (laz) suppressors of autoimmunity-triggered PCD in the Arabidopsis thaliana mutant accelerated cell death11 (acd11) and demonstrated that the cell death phenotype is due to ectopic activation of the LAZ5 NB-LRR. We report here that laz4 is mutated in one of three VACUOLAR PROTEIN SORTING35 (VPS35) genes. We verify that LAZ4/VPS35B is part of the retromer complex, which functions in endosomal protein sorting and vacuolar trafficking. We show that VPS35B acts in an endosomal trafficking pathway and plays a role in LAZ5-dependent acd11 cell death. Furthermore, we find that VPS35 homologs contribute to certain forms of NB-LRR protein-mediated autoimmunity as well as pathogen-triggered HR. Finally, we demonstrate that retromer deficiency causes defects in late endocytic/lytic compartments and impairs autophagyassociated vacuolar processes. Our findings indicate important roles of retromer-mediated trafficking during the HR; these may include endosomal sorting of immune components and targeting of vacuolar cargo.