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 α-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 (ΔVdFtr1) and complemented (ComVdFtr1) mutants of the VdFtr1 gene were obtained via homologous recombination. The biological characteristics and pathogenicity were compared between WT, ΔVdFtr1, and ComVdFtr1 mutants. The results indicate that knockout of VdFtr1 (ΔVdFtr1) 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 ΔVdFtr1 was dramatically attenuated. All impaired phenotypes of ΔVdFtr1 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 α-1,6-Mannosyltransferase (OCH1) regulated microsclerotia formation and pathogenicity signal pathway.