A Colletotrichum tabacum Effector Cte1 Targets and Stabilizes NbCPR1 to Suppress Plant Immunity

Abstract

Colletotrichum tabacum, causing anthracnose in tobacco, is a notorious 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 upregulated in the biotrophic stage. We found that Cte1 depresses plant cell death initiated by BAX and inhibits reactive oxygen species (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. Our study shows that Cte1 suppresses plant immunity to facilitate C. tabacum infection by intervening in the native function of NbCPR1. [Graphic: see text] The author(s) have dedicated the work to the public domain under the Creative Commons CC0 “No Rights Reserved” license by waiving all of his or her rights to the work worldwide under copyright law, including all related and neighboring rights, to the extent allowed by law, 2024.

Keywords

• anthracnose
• fungus
• Nicotiana benthamiana
• plant resistance
• ROS