The State Key Laboratory for Biology of Plant Disease and Insect Pests, Institute of Plant Protection, Chinese Academy of Agricultural Sciences, Beijing, China.
Key Laboratory of Control of Biological Hazard Factors (Plant Origin) for Agri-product Quality and Safety, Ministry of Agriculture, Institute of Plant Protection, Chinese Academy of Agricultural Sciences, Beijing, China.
J Exp Bot. 2019 Jan 7;70(2):613-626. doi: 10.1093/jxb/ery351.
Alt a 1 family proteins (AA1s) have only been observed in the Dothideomycetes and Sordariomycetes classes of fungi, and their biological functions have remained poorly understood. Verticillium dahliae, a soil-borne pathogen that causes plant wilt disease, secretes hundreds of proteins during the process of pathogenic infection, including the AA1 member PevD1. In this study, we found that the pevd1 transcript was present in all of the hosts studied (cotton, Arabidopsis, tomato, and tobacco) and showed elevated expression throughout the infection process. Furthermore, pevd1 knockout mutants displayed attenuated pathogenicity compared with the wild-type (WT) strain and complemented strains in hosts. A partner protein of PevD1, pathogenesis-related protein 5 (PR5)-like protein GhPR5, was isolated from cotton (Gossypium hirsutum) plants by co-purification assays, and the PevD1-GhPR5 interaction was determined to be localized in the C-terminus (PevD1b, amino acids residues 113-155) by pull-down and yeast two-hybrid techniques. Re-introduction of the pevd1b gene into a pevd1 knockout mutant resulted in restoration of the virulence phenotype to WT levels. In addition, PevD1b, which is similar to PevD1, decreased the antifungal activity of GhPR5 in vitro. Our findings reveal an infection strategy in which V. dahliae secretes PevD1 to inhibit GhPR5 antifungal activity in order to overcome the host defence system.
A1 家族蛋白(AA1s)仅在子囊菌门和盘菌门真菌中观察到,其生物学功能仍知之甚少。黄萎病菌是一种土传病原体,可引起植物萎蔫病,在致病感染过程中会分泌数百种蛋白质,包括 AA1 成员 PevD1。在这项研究中,我们发现 pevd1 转录本存在于所有研究的宿主(棉花、拟南芥、番茄和烟草)中,并在整个感染过程中表现出高水平的表达。此外,与野生型(WT)菌株和宿主中的互补菌株相比,pevd1 敲除突变体表现出较弱的致病性。PevD1 的一个伴侣蛋白,与病程相关蛋白 5(PR5)类似的蛋白 GhPR5,通过共纯化试验从棉花(Gossypium hirsutum)植物中分离出来,通过下拉和酵母双杂交技术确定 PevD1-GhPR5 相互作用定位于 C 末端(PevD1b,氨基酸残基 113-155)。将 pevd1b 基因重新导入 pevd1 敲除突变体中,导致其毒力表型恢复到 WT 水平。此外,类似于 PevD1 的 PevD1b 体外降低了 GhPR5 的抗真菌活性。我们的发现揭示了一种感染策略,即黄萎病菌分泌 PevD1 抑制 GhPR5 的抗真菌活性,以克服宿主防御系统。