Reveals how effector CREP1 regulates host plant immunity, suggesting new insights into endophyte interactions.
Pathogen effectors mediate infection and pathogenesis, and extensive research has been conducted on this topic. In contrast, studies on endophyte effectors remain limited, and their functions and mechanisms of action are still not well understood. Here, we report a novel effector identified from the endophytic Fusarium lateritium. Knockout of this effector reduced the colonization rate of the endophyte in the host plant by approximately 70%; therefore, we named it Colonization-Related Effector Protein 1 (CREP1). We found that CREP1 strongly activates host plant immunity and induces cell necrosis in Nicotiana benthamiana leaves. Disruption of CREP1 resulted in significant downregulation of immune defense-related genes in the host plant, accompanied by an approximately 50% decrease in the plant growth-promoting ability of the endophytic fungus. Further investigation revealed that CREP1 interacts with the plant cell-surface recognition receptor protein NbEIX2 to regulate plant immunity. These findings demonstrate that CREP1 is a necrosis-inducing effector in F. lateritium that modulates plant immunity through its interaction with NbEIX2, affecting the colonization and growth-promoting capacity of the endophytic fungus in plants.
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He et al. (2026) studied this question.
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