Wang Shilong, Zhang Yating, Qu Lili, Zhou Zengran, Zhai Hongyang, Wei Songhong, Wang Yan
Department of Plant Pathology, College of Plant Protection, Shenyang Agricultural University, Shenyang 110866, China.
Liaoning Provincial Plant Protection and Quarantine Station, Shenyang 110034, China.
Int J Mol Sci. 2025 Mar 25;26(7):2979. doi: 10.3390/ijms26072979.
Rice false smut, caused by , is one of the three major rice diseases in China. It not only seriously affects the rice yield and quality but also endangers human and animal health. Studying the pathogenic mechanism of has important theoretical significance and application value for clarifying the infection characteristics of the pathogen and cultivating disease-resistant varieties. Plant pathogenic fungi utilize secreted effectors to suppress plant immune responses, which can function in the apoplast or within host cells and are likely glycosylated. However, the posttranslational regulation of these effectors remains unexplored. Deletion of ΔUvALG led to the cessation of secondary infection hyphae growth and a notable decrease in virulence. We observed that ΔUvALG mutants triggered a significant increase in reactive species production within host cells, akin to ALG mutants, which plays a crucial role in halting the growth of infection hyphae in the mutants. ALG functions by sequestering chitin oligosaccharides to prevent their recognition by the rice chitin elicitor, thereby inhibiting the activation of innate immune responses, including reactive species production. Our findings reveal that ALG3 possesses three N-glycosylation sites, and the simultaneous Alg-mediated N-glycosylation of each site is essential for maintaining protein stability and chitin-binding activity, both of which are critical for its effector function. These outcomes underscore the necessity of the Alg-mediated N-glycosylation of ALG to evade host innate immunity.
由[未提及具体病原体名称]引起的稻曲病是中国三大水稻病害之一。它不仅严重影响水稻产量和品质，还危及人类和动物健康。研究[未提及具体病原体名称]的致病机制对于阐明病原体的感染特性和培育抗病品种具有重要的理论意义和应用价值。植物病原真菌利用分泌的效应子来抑制植物免疫反应，这些效应子可在质外体或宿主细胞内发挥作用，并且可能是糖基化的。然而，这些效应子的翻译后调控仍未得到探索。缺失ΔUvALG导致次生感染菌丝生长停止，毒力显著下降。我们观察到，ΔUvALG突变体引发宿主细胞内活性物质产生显著增加，类似于ALG突变体，后者在阻止突变体中感染菌丝生长方面起关键作用。ALG通过螯合几丁质寡糖发挥作用，以防止水稻几丁质激发子对其识别，从而抑制包括活性物质产生在内的先天免疫反应的激活。我们的研究结果表明，ALG3具有三个N-糖基化位点，每个位点同时进行的Alg介导的N-糖基化对于维持蛋白质稳定性和几丁质结合活性至关重要，这两者对其效应子功能都至关重要。这些结果强调了Alg介导的ALG的N-糖基化对于逃避宿主先天免疫的必要性。
