VdPLP, A Patatin-Like Phospholipase in Verticillium dahliae, Is Involved in Cell Wall Integrity and Required for Pathogenicity

文献类型： 外文期刊

第一作者： Qi, Xiliang

作者： Qi, Xiliang;Li, Xiaokang;Guo, Huiming;Cheng, Hongmei;Qi, Xiliang;Li, Xiaokang;Guo, Ning

作者机构：

关键词： Verticillium dahliae; patatin-like phospholipases; cell wall integrity; pathogenicity

期刊名称：GENES （ 影响因子：4.096； 五年影响因子：4.339 ）

ISSN： 2073-4425

年卷期： 2018 年 9 卷 3 期

页码：

收录情况： SCI

摘要： The soil-borne ascomycete fungus Verticillium dahliae causes vascular wilt disease and can seriously diminish the yield and quality of important crops. Functional analysis of growthand pathogenicity-related genes is essential for revealing the pathogenic molecular mechanism of V. dahliae. Phospholipase is an important virulence factor in fungi that hydrolyzes phospholipids into fatty acid and other lipophilic substances and is involved in hyphal development. Thus far, only a few V. dahliae phospholipases have been identified, and their involvement in V. dahliae development and pathogenicity remains unknown. In this study, the function of the patatin-like phospholipase gene in V. dahliae (VdPLP, VDAG_00942) is characterized by generating gene knockout and complementary mutants. Vegetative growth and conidiation of VdPLP deletion mutants (D VdPLP) were significantly reduced compared with wild type and complementary strains, but more microsclerotia formed. The D VdPLP mutants were very sensitive to the cell-wall-perturbing agents: calcofluor white (CFW) and Congo red (CR). The transcriptional level of genes related to the cell wall integrity (CWI) pathway and chitin synthesis were downregulated, suggesting that VdPLP has a pivotal role in the CWI pathway and chitin synthesis in V. dahliae. D VdPLP strains were distinctly impaired in in their virulence and ability to colonize Nicotiana benthamiana roots. Our results demonstrate that VdPLP regulates hyphal growth and conidial production and is involved in stabilizing the cell wall, thus mediating the pathogenicity of V. dahliae.

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