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MoWhi2 Participates in Mitophagy and Pathogenesis by Modulating MoAti1 Protein Level in Magnaporthe Oryzae

  1. School of Life Science, Hubei University, Wuhan 430062, China; State Key Laboratory of Rice Biology and Breeding, China National Rice Research Institute, Hangzhou 311400, China; National Joint Local Engineering Laboratory for High-Efficient Preparation of Biopesticide, College of Forestry and Biotechnology, Zhejiang Agriculture and Forestry University, Hangzhou 311300, China. #These authors contributed equally to this work
  • Contact: KOU Yanjun; LIU Li; SHI Huanbin
  • Supported by:

    This study was supported by the National Natural Science Foundation of China (Grant No. 32470208), Zhejiang Provincial Natural Science Foundation of China (Grant Nos. R24C140014 and LD25C140001), and National Key R&D Program of China (Grant No. 2022YFD1401500). This project was also supported by the Central Public-interest Scientific Institution Basal Research Fund (Grant No. Y2025YC94) and the Agricultural Sciences and Technologies Innovation Program (Grant No. CAAS-CSCB-202301). We thank Rice-Pathogen Interaction group at China National Rice Research Institute for providing vector resources, useful discussion, and suggestions.

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Abstract: Rice blast caused by the fungus Magnaporthe oryzae is one of the most devastating diseases affecting rice production. It was previously demonstrated that MoWHI2 is indispensable for mitophagy and full virulence in M. oryzae, yet the molecular mechanisms underlying its control of mitophagy was unresolved. In this study, we found that MoWhi2 interacts with MoAti1, a SUN family protein that mediates mitophagy by recruiting autophagy-associated protein MoAtg8. Phenotypic analysis showed that the defects of ΔMowhi2/ΔMoati1 mutant in growth, conidiation, and pathogenicity were comparable to those of ΔMoati1, but more severe than those of ΔMowhi2. Furthermore, compared with wild type, the ΔMowhi2/ΔMoati1 exhibited a lower mitophagy level similar to the single deletion mutants ΔMowhi2 or ΔMoati1. In addition, deletion of MoWHI2 resulted in decreased protein level of MoAti1, suggesting that MoWhi2 might regulate mitophagy by modulating the protein level of MoAti1. Due to absence of MoWhi2 orthologues in both rice and humans, we employed host-induced gene silencing (HIGS) targeting MoWHI2 in rice plants; the resultant transgenic rice lines displayed resistance to blast without agronomic penalties. Collectively, our data established that MoWhi2 regulates the mitophagy and pathogenicity of M. oryzae by interacting with MoAti1, and it could serve as a target for rice blast control strategies.

Key words: rice blast, pathogenesis, fungal disease, mitophagy, Whi2