Experimental study reveals fungal effector CfCFEM19 suppresses immunity by targeting membrane chitinase ChtBD1-P1 in Camellia oleifera, highlighting a key mechanism for anthracnose virulence.
Plants defend against pathogen invasion by synthesizing defense-related enzymes. Pathogens promote their infection by secreting effectors that suppress plant defense responses. However, little is known about how CFEM effector proteins from pathogenic fungi act to suppress plant immunity. In this study, we identified a secreted CFEM effector protein CfCFEM19 from Colletotrichum fructicola . We found that the CfCFEM19 can suppress leaf necrosis in Nicotiana benthamiana plants that is caused by BAX or INF1. Moreover, overexpression of CfCFEM19 significantly increases the susceptibility of plants to pathogenic fungi. The deletion of the CfCFEM19 gene, although it did not significantly affect mycelial growth, response to various stresses, and appressorium formation of C. fructicola , reduced the virulence of the fungus. Notably, CfCFEM19 interacts with the chitinase ChtBD1-P1, which is localized in the cell membrane in Camellia oleifera . ChtBD1-P1 can inhibit the infection of C. fructicola , while CfCFEM19 can affect the function of ChtBD1-P1. These findings indicate that CfCFEM19, as an important pathogenic factor in C. fructicola ,. It can weaken the resistance of C. oleifera to C. fructicola by targeting ChtBD1-P1. This study provides a foundation for the development of precise and highly effective green pesticides against C. oleifera anthracnose in the future, as well as important insights into the mechanisms of fungal infection and plant-microbe interactions.
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Chen et al. (2026) studied this question.
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