Open AccessBRASSINOSTEROID‐SIGNALLING KINASES 7 and 8 associate with the FLS2 immune receptor and are required for flg22‐induced PTI responses
Author(s) -
Majhi Bharat Bhusan,
Sobol Guy,
Gachie Sarah,
Sreeramulu Shivakumar,
Sessa Guido
Publication year - 2021
Publication title -
molecular plant pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.945
H-Index - 103
eISSN - 1364-3703
pISSN - 1464-6722
DOI - 10.1111/mpp.13062
Subject(s) - brassinosteroid , signalling , biology , kinase , immune system , signalling pathways , microbiology and biotechnology , protein serine threonine kinases , receptor , signal transduction , immunology , arabidopsis , protein kinase a , genetics , gene , mutant
Pattern‐triggered immunity (PTI) is typically initiated in plants by recognition of pathogen‐ or damage‐associated molecular patterns (PAMP/DAMPs) by cell surface‐localized pattern recognition receptors (PRRs). Here, we investigated the role in PTI of Arabidopsis thaliana brassinosteroid‐signalling kinases 7 and 8 (BSK7 and BSK8), which are members of the receptor‐like cytoplasmic kinase subfamily XII. BSK7 and BSK8 localized to the plant cell periphery and interacted in yeast and in planta with FLS2, but not with other PRRs. Consistent with a role in FLS2 signalling, bsk7 and bsk8 single and bsk7,8 double mutant plants were impaired in several immune responses induced by flg22, but not by other PAMP/DAMPs. These included resistance to Pseudomonas syringae and Botrytis cinerea , reactive oxygen species accumulation, callose deposition at the cell wall, and expression of the defence‐related gene PR1 , but not activation of MAP kinases and expression of the FRK1 and WRKY29 genes. bsk7 , bsk8 , and bsk7,8 plants also displayed enhanced susceptibility to P. syringae and B. cinerea . Finally, BSK7 and BSK8 variants mutated in their myristoylation site or in the ATP‐binding site failed to complement defective phenotypes of the corresponding mutants, suggesting that localization to the cell periphery and kinase activity are critical for BSK7 and BSK8 functions. Together, these findings demonstrate that BSK7 and BSK8 play a role in PTI initiated by recognition of flg22 by interacting with the FLS2 immune receptor.