Tomato LysM receptor kinase 4 mediates chitin-elicited fungal resistance in both leaves and fruit

Abstract

Fungal infection is a major cause of crop and fruit losses. Recognition of chitin, a component of fungal cell walls, endows plants with enhanced fungal resistance. Here, we found that mutation of tomato LysM receptor kinase 4 (SlLYK4) and chitin elicitor receptor kinase 1 (SlCERK1) impaired chitin-induced immune responses in tomato leaves. Compared with the wild type, <i>sllyk4</i> and <i>slcerk1</i> mutant leaves were more susceptible to <i>Botrytis cinerea</i> (gray mold). SlLYK4 extracellular domain showed strong binding affinity to chitin, and the binding of SlLYK4 induced SlLYK4-SlCERK1 association. Remarkably, qRT-PCR analysis indicated that <i>SlLYK4</i> was highly expressed in tomato fruit, and <i>β-GLUCURONIDASE</i> (<i>GUS</i>) expression driven by the <i>SlLYK4</i> promoter was observed in tomato fruit. Furthermore, <i>SlLYK4</i> overexpression enhanced disease resistance not only in leaves but also in fruit. Our study suggests that chitin-mediated immunity plays a role in fruit, providing a possible way to reduce fungal infection-related fruit losses by enhancing the chitin-induced immune responses.