The lectin receptor kinase-VI.2 is required for priming and positively regulates Arabidopsis pattern-triggered immunity

Plant cells can be sensitized toward a subsequent pathogen attack by avirulent pathogens or by chemicals such as beta aminobutyric acid (BABA). This process is called priming. Using a reverse genetic approach in Arabidopsis thaliana we demonstrate that the BABA responsive L type lectin receptor kinase VI. 2 (LecRK VI.2) contributes to disease resistance against the hemibiotrophic Pseudomonas syringae and the necrotrophic Pectobacterium carotovorum bacteria. Accordingly LecRK VI.2 mRNA levels increased after bacterial inoculation or treatments with microbe associated molecular patterns (MAMPs). We also show that LecRK VI.2 is required for full activation of pattern triggered immunity (PTI); notably lecrk VI.2 1 mutants show reduced upregulation of PTI marker genes impaired callose deposition and defective stomatal closure. Overexpression studies combined with genome wide microarray analyses indicate that LecRK VI.2 positively regulates the PTI response. LecRK VI.2 is demonstrated to act upstream of mitogen activated protein kinase signaling but independently of reactive oxygen production and BOTRYTIS INDUCED KINASE1 phosphorylation. In addition complex formation between the MAMP receptor FLAGELLIN SENSING2 and its signaling partner BRASSINOSTEROID INSENSITIVE1 ASSOCIATED KINASE1 is observed in flg22 treated lecrk VI.2 1 mutants. LecRK VI.2 is also required for full BABA induced resistance and priming of PTI. Our work identifies LecRK VI.2 as a novel mediator of the Arabidopsis PTI response and provides insight into molecular mechanisms governing priming.