Tomato B-cell lymphoma2 (Bcl2)-associated athanogene 5 (SlBAG5) contributes negatively to immunity against necrotrophic fungus Botrytis cinerea through interacting with SlBAP1 and modulating catalase activity.

The evolutionarily conserved and multifunctional B-cell lymphoma2 (Bcl2)-associated athanogene proteins (BAGs), serving as co-chaperone regulators, play a pivotal role in orchestrating plant stress responses. In this study, the possible involvement of tomato SlBAG genes in resistance to Botrytis cinerea was examined. The SlBAG genes respond with different expression change patterns to B. cinerea and defense signaling hormones. SlBAG proteins are individually differentially localized to the nucleus, mitochondria, cytoplasm, endoplasmic reticulum (ER), or vacuole. Silencing of SlBAG5 enhanced immunity to B. cinerea, while overexpression weakened it, affecting Botrytis-induced JA/ET defense gene expression and JA levels. Chitin-induced ROS burst and expression of PTI marker genes SlPTI5 and SlLRR22 were strengthened in SlBAG5-silenced plants but were weakened in SlBAG5-overexpressing plants (SlBAG5-OE) plants. SlBAG5 interacts with BON1 ASSOCIATED PROTEIN 1 (SlBAP1) through its BAG domain, and the stability of SlBAP1 depends on the presence of SlBAG5. Silencing of SlBAP1 conferred increased resistance to B. cinerea through increased expression of JA/ET signaling and defense genes. SlBAP1 functions by recruiting and boosting SlCAT3 activity to remove HO. The findings suggest that SlBAG5 suppresses tomato immunity to B. cinerea by stabilizing SlBAP1, which modulates ROS scavenging and acts as a negative regulator of immunity.