SlTCP16 confers disease resistance in tomato via a dual regulatory mechanism involving transcriptional activation and protein interaction with Sl4CL3.

Our study revealed that SlTCP16 can transcriptional activation and interaction with Sl4CL3, thereby enhancing the tomato's resistance toPstDC3000. This resistance is associated with an increased accumulation of lignin. Lignin deposition serves as a critical physical barrier against bacterial pathogens. However, the precise regulatory networks orchestrating this defense response in tomato remain incompletely understood. We identify the transcription factor SlTCP16 as a novel positive regulator of tomato immunity against Pseudomonas syringae pv. tomato (Pst DC3000). We show that Pst DC3000 infection strongly induces SlTCP16 expression. Functionally, SlTCP16 overexpression significantly reduced reactive oxygen species (ROS) accumulation and bolstered disease resistance, while SlTCP16 knockout mutants showed the opposite performance. Mechanistically, we uncover a dual regulatory mode, SlTCP16 not only directly activates the transcription of the lignin biosynthetic gene Sl4CL3 by binding to its promoter but also physically interacts with the Sl4CL3 protein. Sl4CL3 acts downstream of SlTCP16, and overexpression of Sl4CL3 enhanced disease resistance in the sltcp16 mutant. Collectively, our data suggest that SlTCP16 contributes to disease resistance by regulating Sl4CL3 through transcriptional activation and protein-protein interaction. This regulatory module is associated with increased lignin accumulation.