| Summary: | Apple canker disease, caused by <i>Valsa mali</i>, is one of the most serious apple tree diseases in China. <i>VmSom1</i> is an important transcription factor that acts on the cyclic adenosine signaling pathway (cAMP/PKA), regulating the growth, development, morphological differentiation, and pathogenic forces of the pathogen. We perform transcriptome analysis of the <i>VmSom1</i> deletion mutant and the wild-type strain 11-175 and identify a significantly differentially expressed gene, <i>VM1G_06867</i>, a zinc finger motif transcription factor in <i>V. mali</i>. In this study, we obtain the <i>VM1G_06867</i> gene using the single deletion mutant via homologous recombination. To determine the relationship between <i>VmSom1</i> and <i>VM1G_06867</i>, we also obtain a double deletion mutant <i>ΔVmSom1/06867</i>. Compared to the wild-type strain 11-175, the single deletion mutant <i>VM1G_06867</i> shows a drastic reduction in growth rate and forms more pycnidia on the PDA medium. Additionally, the growth of the mutant is inhibited by SDS, Congo red, and fluorescent brighteners. In comparison to the single deletion mutant <i>VmSom1</i>, the double deletion mutant <i>ΔVmSom1/06867</i> shows no significant change in growth or conidiation and is unable to produce conidia. The growth rate is significantly increased in Congo red, NaCl, and Sorbitol mediums. These results demonstrate that <i>VM1G_06867</i> plays important roles in growth, pathogenicity, asexual development, and maintenance of cell wall integrity. <i>VM1G_06867</i> can recover osmotic stress and cell wall integrity defects caused by the deletion of <i>VmSom1</i>, as well as restore the loss of pathogenicity caused by the deletion of the <i>VmSom1</i> gene, but not completely.
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