Abstract

Simple SummaryPlants are constantly threatened by disease-causing bacteria. To defend themselves, they rely on sensors on their cell surfaces that detect invading germs and turn on immune responses. In this study, we asked which plant genes are switched on quickly during infection and whether any of them could be used to make crops more resistant. We discovered a gene calledReceptor Kinase 3(orRK3for short) in the model plantArabidopsis. When this gene is active, it helps the plant mount a stronger defense against bacteria. Surprisingly, RK3 works in an unusual way: it does not need the typical “kinase” activity that most similar defense proteins require. Instead, it simply attaches to the main immune sensor complex and boosts its signaling. Importantly, when we put the sameRK3gene into tomato plants, they also became more resistant to bacterial infection. Our findings reveal a new trick that plants use to fight diseases, and they suggest thatRK3could be a useful tool for breeding or engineering crops with better disease resistance, helping to reduce the use of chemical pesticides.Lectin receptor-like kinases (LecRLKs) are a large subfamily of receptor-like kinases (RLKs), and their N-terminal lectin domain is predicted to reversibly bind to carbohydrates. Within this family, G-type LecRLKs represent a distinct subclass defined by an extracellular S-locus glycoprotein (SLG) domain, which was originally identified for its role in governing self-incompatibility inBrassicaspecies. Emerging evidence suggests that G-type LecRLKs are involved in plant immunity; however, only a small fraction have been functionally characterized, leaving the roles of most family members largely unknown. In this study, we identifiedRK3(Receptor Kinase 3) as the most strongly induced gene within the G-type LecRLK clade VI upon infection withPseudomonas syringaepv.tomatoDC3000 (PstDC3000). Through both gain- and loss-of-function analyses, we demonstrated that RK3 positively regulates flg22-i