EXTRA LARGE G-PROTEIN 2 (XLG2) mediates cell death and hyperimmunity via a novel, apoplastic ROS-independent pathway in Arabidopsis thaliana
Autor: | Marcel Wiermer, Patrick Fasshauer, Volker Lipka, Ronja Hacke, Anna-Lena Gippert, Julia Anders, Samuel Kroll, Marnie Stolze, Melina Ayaka Schwier, Elena Petutschnig, Christopher Meusel |
---|---|
Rok vydání: | 2021 |
Předmět: |
0106 biological sciences
0303 health sciences Programmed cell death biology Chemistry G protein Mutant biology.organism_classification 01 natural sciences Cell biology 03 medical and health sciences Cell surface receptor Arabidopsis Arabidopsis thaliana Phosphorylation Signal transduction 030304 developmental biology 010606 plant biology & botany |
DOI: | 10.1101/2021.10.08.463358 |
Popis: | Heterotrimeric G-Proteins are signal transduction complexes comprised of three subunits, Gα, Gβ and Gγ, and are involved in many aspects of plant life. The non-canonical Gα subunit XLG2 mediates PAMP-induced ROS generation and immunity downstream of PRRs. A mutant of the chitin receptor component CERK1, cerk1-4, maintains normal chitin signalling capacity, but shows excessive cell death upon infection with powdery mildews. We identified XLG2 mutants as suppressors of the cerk1-4 phenotype.We generated stably transformed Arabidopsis lines expressing Venus-XLG2 and numerous mutated variants. These were analysed by confocal microscopy, Western blotting and pathogen infection. We also crossed cerk1-4 with several mutants involved in immunity and analysed their phenotype. Phosphorylation of XLG2 was investigated by quantitative proteomics.Mutations in XLG2 complex partners AGB1 and AGG1 have a partial cerk1-4 suppressor effect. The cerk1-4 phenotype is independent of NADPH oxidase-generated ROS, BAK1 and SOBIR1, but requires PUB2. XLG2 mediates cerk1-4 cell death at the cell periphery. Integrity of the XLG2 N-terminal domain, but not its phosphorylation, is essential for correct XLG2 localisation and cerk1-4 signalling.Our results suggest that XLG2 transduces signals from an unknown cell surface receptor that activates an apoplastic ROS-independent cell death pathway in Arabidopsis. |
Databáze: | OpenAIRE |
Externí odkaz: |