The tomato cytoplasmic receptor-like kinase TPK09 mediates resistance to Botrytis cinerea and tolerance to light-induced stress.

Plant responses to pathogens often rely on receptor-like cytoplasmic kinases (RLCKs) that mediate signaling through interactions with receptor kinases and downstream components. Here, we studied the tomato RLCK, TPK1b Related Protein Kinase (TPK09), and demonstrate its function in integrating defense with light stress responses. Tomato tpk09 mutants exhibited increased susceptibility to Botrytis cinerea and the vascular pathogen Fusarium oxysporum, whereas transgenic expression of TPK09 enhanced resistance to Botrytis. Disease severity in tpk09 mutants was elevated under light-emitting diode (LED) compared to fluorescent light (FL). In the absence of infection, mutants displayed severe necrosis and elevated H2O2 accumulation under LED lighting. TPK09 interacts with the cell death-inducing transglycosylase BcCrh1 from Botrytis. Consistently, TPK09 suppresses cell death triggered by Botrytis infection as well as by BcCrh1 expression. Loss of TPK09 abolished pathogen-induced expression of the tomato suppressor of cell death BAX INHIBITOR-LIKE1 and compromised chitin- and flg22-triggered reactive oxygen species (ROS) accumulation and immune gene activation. Further, TPK09 mitigates damage to the photosynthetic system under elevated light stress, demonstrated by a decrease in the effective photochemical quantum yield of PSII and electron transport rate in the mutant plants. In addition, TPK09 expression is induced by light but suppressed under dark conditions, and the mutant seedlings were insensitive to hypocotyl growth responses to light. RNA sequencing (RNA-seq) studies suggest TPK09 is required for expression of genes involved in light harvesting, photosynthesis, and stress response functions. Collectively, TPK09 plays a key role in enhancing fungal resistance, maintaining the homeostasis of the photosynthetic apparatus and ROS levels, and mitigating photooxidative damage.