ABSTRACT
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.
Competing Interest Statement
The authors have declared no competing interest.