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Ferric ion permease gene VdFtr1 regulates the formation of microsclerotia and pathogenicity in Verticillium dahliae

文献类型： 外文期刊

作者： Yang, Jianfeng 1 ; Feng, Yitong 1 ; Zhang, Xiaoluo 1 ; Gao, Jing 1 ; Cao, Qingqin 4 ; Xiao, Tingting 4 ; Zhao, Jun 1 ; Zhang, Jian 1 ;

作者机构： 1.Inner Mongolia Agr Univ, Coll Hort & Plant Protect, Hohhot 010019, Peoples R China

2.Agr & Anim Husb Technol Extens Ctr Inner Mongolia, Hohhot 010013, Peoples R China

3.Inner Mongolia Acad Agr & Anim Husb Sci, Hohhot 010031, Peoples R China

4.Beijing Agr Univ, Coll Plant Sci Technol, Beijing 102206, Peoples R China

关键词： Verticillium dahliae; Iron ion permease gene; Microsclerotia; Pathogenicity

期刊名称：PHYSIOLOGICAL AND MOLECULAR PLANT PATHOLOGY （ 影响因子：3.3； 五年影响因子：3.2 ）

ISSN： 0885-5765

年卷期： 2025 年 136 卷

页码：

收录情况： SCI

摘要： Verticillium dahliae is a soilborne plant pathogen that infects over 660 plant species, causing Verticillium wilt (VW). Microsclerotia are specialized latent structures generated in the late infection stage of V. dahliae, serving as the primary inoculum for many hosts. Our previous research demonstrated that alpha-1,6-Mannosyltransferase (VdOCH1) regulates microsclerotia formation and pathogenicity in V. dahliae. Subsequently, transcriptome analysis comparing the VdOCH1 gene knockout mutant and wild-type (WT) strain of V. dahliae revealed significant alterations in the expression profiles of 1563 genes in the knockout mutant, with 739 genes upregulated and 824 downregulated. The VdFtr1 (VDAG_09918) gene was selected for further function analysis based on its significantly down-regulated knockout mutant. The knockout (Delta VdFtr1) and complemented (ComVdFtr1) mutants of the VdFtr1 gene were obtained via homologous recombination. The biological characteristics and pathogenicity were compared between WT, Delta VdFtr1, and ComVdFtr1 mutants. The results indicate that knockout of VdFtr1 (Delta VdFtr1) significantly reduced conidial production and inhibited microsclerotial formation. Concurrently, the expression levels of genes involved in melanin formation and microsclerotium formation were down-regulated, leading to a markedly diminished ability for microsclerotia formation. Also, the pathogenicity of the Delta VdFtr1 was dramatically attenuated. All impaired phenotypes of Delta VdFtr1 could be restored in ComVdFtr1, in which the full-length VdFtr1 gene was complemented in a knockout mutant. In conclusion, VdFtr1, encoded iron transporter permease, functions as a downstream target in alpha-1,6-Mannosyltransferase (OCH1) regulated microsclerotia formation and pathogenicity signal pathway.

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