Department of Plant Pathology, College of Plant Protection, Nanjing Agricultural University/Key Laboratory of Monitoring and Management of Crop Diseases and Pest Insects, Ministry of Education, Nanjing, Jiangsu, China.
Safety and Quality, Ministry of Agriculture and Rural Affairs/Key Laboratory for Agro-product Safety Risk Evaluation (Nanjing), Ministry of Agriculture and Rural Affairs/Collaborative Innovation Center for Modern Grain Circulation and Safety/Institute of Food Safety and Nutrition, Jiangsu Academy of Agricultural SciencesJiangsu Key Laboratory for Food Quality and Safety-State Key Laboratory Cultivation Base, Ministry of Science and Technology/Key Laboratory for Control Technology and Standard for Agro-product, Nanjing, Jiangsu, China.
Virulence. 2022 Dec;13(1):764-780. doi: 10.1080/21505594.2022.2066611.
Autophagy is the main intracellular degradation system by which cytoplasmic materials are transported to and degraded in the vacuole/lysosome of eukaryotic cells, and it also controls cellular differentiation and virulence in a variety of filamentous fungi. However, the contribution of the autophagic pathway to fungal development and pathogenicity in the important maize pathogen and mycotoxigenic fungus is still unknown. In this study, we characterized two autophagy-related proteins, FvAtg4 and FvAtg8. The deletion mutants Δ and Δ were impaired in autophagosome formation, aerial hyphal formation, sexual growth, lipid turnover, pigmentation and fungal virulence. Interestingly, Δ and Δ were defective in fumonisin B1 (FB1) synthesis, which may have resulted from decreased intracellular levels of alanine in the mutants. Our results indicate that FvAtg4 and FvAtg8 contribute to pathogenicity by regulating the autophagic pathway to control lipid turnover, fumonisin biosynthesis, and pigmentation during its infectious cycle.
自噬是真核细胞内主要的细胞内降解系统,通过该系统细胞质物质被运输到液泡/溶酶体中并被降解,它还控制着各种丝状真菌的细胞分化和毒力。然而,自噬途径对重要的玉米病原体和产毒真菌的真菌发育和致病性的贡献仍然未知。在本研究中,我们对两个自噬相关蛋白 FvAtg4 和 FvAtg8 进行了表征。Δ和Δ缺失突变体在自噬体形成、气生菌丝形成、有性生长、脂质周转、色素形成和真菌毒力方面受损。有趣的是,Δ和Δ在腐马菌素 B1 (FB1) 合成中存在缺陷,这可能是由于突变体中丙氨酸的细胞内水平降低所致。我们的结果表明,FvAtg4 和 FvAtg8 通过调节自噬途径来控制脂质周转、腐马菌素生物合成和在感染周期中的色素形成,从而有助于致病性。