CaEch1-mediated mitophagy regulates vegetative growth, conidiation, appressorium formation, and pathogenicity in Colletotrichum camelliae
2025
Shuai Meng | Meng Xiong | Longjun Cheng | Li Wang | Ya Chen | Chaoxi Luo | Shufen Chao
Abstract Anthracnose, caused by Colletotrichum camelliae, poses a significant threat to the yield and quality of Camellia oleifera. Mitophagy, a selective form of autophagy, is crucial in maintaining mitochondrial quality and intracellular homeostasis. To date, an optimized experimental system for studying mitophagy in C. camelliae has yet to be established, and the role of mitophagy in the pathogenesis of C. camelliae remains unclear. Here, we characterized the function of CaEch1, a homolog of Magnaporthe oryza MoEch1, in the anthracnose fungus C. camelliae. Our findings indicate that mitochondria-localized CaEch1, plays a vital role for mitophagy in C. camelliae. Also, the CaEch11-29-GFP could serve as a reliable marker for monitoring mitophagy in C. camelliae. Additionally, the knockout of CaECH1 resulted in defects in fungal growth, conidiation, and appressorium formation. Pathogenicity assays further revealed that knockout of CaECH1 significantly reduced the virulence of C. camelliae. In summary, our research underscores the importance of CaEch1 in growth, conidiation, appressorium formation, and virulence in C. camelliae. This suggests its potential as a marker for mitophagy and provides valuable insights for developing new fungicides targeting anthracnose.
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