A Colletotrichum tabacum effector Cte1 targets and stabilizes NbCPR1 to suppress plant immunity.

Colletotrichum tabacum, causing anthracnose in tobacco, is a disreputable plant pathogen threatening tobacco production globally. The underlying mechanisms of C. tabacum effectors that interfere with plant defense are not well known. Here, we identified a novel effector Cte1 from C. tabacum, and its expression was up-regulated in the biotrophic stage. We found that Cte1 depresses plant cell death initiated by BAX and inhibits ROS bursts triggered by flg22 and chitin in Nicotiana benthamiana. The CTE1 knockout mutants decrease the virulence of C. tabacum to N. benthamiana, and the Cte1 transgenic N. benthamiana increase susceptibility to C. tabacum, verifying that Cte1 is involved in the pathogenicity of C. tabacum. We demonstrated that Cte1 interacted with NbCPR1, a Constitutive expresser of Plant Resistance (CPR) protein in plants. Silencing of NbCPR1 expression attenuated the infection of C. tabacum, indicating that NbCPR1 negatively regulates plant immune responses. Cte1 stabilizes NbCPR1 in N. benthamiana. Together, our study showed that Cte1 suppresses plant immunity to facilitate C. tabacum infection by intervening in the native function of NbCPR1.