Nature Communications | 中科院微生物所郭惠珊组揭示大丽轮枝菌致病新机制

大丽轮枝菌引起的棉花黄萎病是一种土传维管束真菌病害，由于病原菌致病机制复杂，病原菌与寄主互作机制不清楚，这成为有效防治该病的关键难题。近年来研究表明，大丽轮枝菌通过分泌大量致病相关毒性蛋白抑制寄主植物的免疫反应，使寄主发病。探究这些毒性蛋白的致病机理及其与寄主的互作机制是该病综合防治及抗病育种的重要基础工作。

近日，中国科学院微生物研究所郭惠珊研究员团队在国际著名期刊Nature Communications发表了题为“DeSUMOylation of a Verticillium dahliae enolase facilitates virulence by derepressing the expression of the effector VdSCP8”的研究论文，揭示了大丽轮枝菌烯醇化酶的去SUMO化通过抑制效应因子VdSCP8的表达从而有助于毒力。

在本研究中，作者从大丽轮枝菌中鉴定了一种小的泛素样修饰因子（SUMO）特异性蛋白酶（VdUlpB），并发现VdUlpB通过从大丽轮枝菌烯醇化酶（VdEno）中去偶联SUMO来促进大丽轮枝菌的毒力。作者鉴定了介导VdEno-SUMO化的五个赖氨酸残基（K96、K254、K259、K313和K434），并且SUMO化VdEno优先定位在细胞核中，在细胞核中它作为转录阻遏物发挥作用以抑制效应因子VdSCP8的表达。重要的是，VdUlpB介导VdEno的去SUMO化促进其细胞质分布，使其能够发挥糖酵解酶的作用。我们的研究揭示了VdUlpB介导的烯醇化酶去SUMO化的复杂致病机制，通过去抑制效应因子的表达来促进大丽轮枝菌的毒力。

原文链接：https://www.nature.com/articles/s41467-023-40384-w/figures/6

A proposed working model for the role of VdEno in regulating the growth and pathogenicity of V. dahliae

The soil-borne fungus Verticillium dahliae, the most notorious plant pathogen of the Verticillium genus, causes vascular wilts in a wide variety of economically important crops. The molecular mechanism of V. dahliae pathogenesis remains largely elusive. Here, we identify a small ubiquitin-like modifier (SUMO)-specific protease (VdUlpB) from V. dahliae, and find that VdUlpB facilitates V. dahliae virulence by deconjugating SUMO from V. dahliae enolase (VdEno). We identify five lysine residues (K96, K254, K259, K313 and K434) that mediate VdEno SUMOylation, and SUMOylated VdEno preferentially localized in nucleus where it functions as a transcription repressor to inhibit the expression of an effector VdSCP8. Importantly, VdUlpB mediates deSUMOylation of VdEno facilitates its cytoplasmic distribution, which allows it to function as a glycolytic enzyme. Our study reveals a sophisticated pathogenic mechanism of VdUlpB-mediated enolase deSUMOylation, which fortifies glycolytic pathway for growth and contributes to V. dahliae virulence through derepressing the expression of an effector.

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