Randomized trial investigates fungal effector CgCAP1's role in reducing apple resistance, indicating significant implications for crop management.
Apple bitter rot, caused by Colletotrichum gloeosporioides, leads to widespread yield loss and quality decline. Fungal virulence effectors are essential determinants of pathogenicity. However, the molecular mechanisms underlying C. gloeosporioides effector-mediated pathogenesis in apple remain largely elusive. Here, we found that the transcription factor MdWRKY100 binds to the promoter of the chitinase gene MdChi5, directly promoting its transcription and thereby improving apple bitter rot resistance. Meanwhile, a VQ-motif containing protein 4-like in apple, MdMVQ4, interacts with MdWRKY100, enhancing apple resistance to C. gloeosporioides. We identified the effector CgCAP1 in C. gloeosporioides via yeast two-hybrid (Y2H) and confirmed its interaction with MdMVQ4 using luciferase complementation imaging, bimolecular fluorescence complementation, and co-immunoprecipitation assays. In addition, knockout and complementation assays in C. gloeosporioides demonstrated that CgCAP1 functions as a critical virulence effector. Furthermore, the interaction of CgCAP1 with MdMVQ4 weakened the interaction between MdMVQ4 and MdWRKY100, leading to a reduction in chitinase activity during C. gloeosporioides infection and reduced apple bitter rot resistance. Together, these findings show how C. gloeosporioides utilizes CgCAP1 to suppress chitinase activity in apple, revealing the molecular interaction between the pathogen and its host.
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Shi et al. (2026) studied this question.
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