The CfMcm1 Regulates Pathogenicity, Conidium Germination, and Sexual Development in <i>Colletotrichum fructicola</i>

附着胞 生物 分生孢子 炭疽菌 菌丝体 炭疽菌 突变体 发芽 微生物学 转录组 毒力 植物 有性生殖 叶斑病 菌丝 基因表达 基因 接种 遗传学 园艺
作者
Wenkui Liu,Lu Han,Jinzhu Chen,Xiaofei Liang,Bo Wang,Mark L. Gleason,Rong Zhang,Guangyu Sun
出处
期刊:Phytopathology [American Phytopathological Society]
卷期号:112 (10): 2159-2173 被引量:1
标识
DOI:10.1094/phyto-03-22-0090-r
摘要

Glomerella leaf spot (GLS), caused by Colletotrichum fructicola, is a severe disease worldwide on apple, causing defoliation, leaf and fruit spot, and substantial yield loss. However, little is known about its molecular mechanisms of pathogenesis. Previous transcriptome analysis revealed that a transcription factor, CfMcm1, was induced during leaf infection. In the present work, expression pattern analysis verified that the CfMcm1 gene was strongly expressed in conidia and early infection. Phenotypic analysis revealed that the gene deletion mutant ΔCfMcm1 lost pathogenicity to apple leaves by inhibiting conidial germination and appressorium formation. In addition to appressorium-mediated pathogenicity, ΔCfMcm1 colonization and hyphal extension in wounded apple fruit was also reduced, and conidial germination mode and conidial color were altered. ΔCfMcm1 displayed impairment of cell wall integrity and response to stress caused by oxidation, osmosis, and an acid environment. Furthermore, the deletion mutant produced fewer and smaller perithecia and no ascospores. In contrast, melanin deposition in mycelia of ΔCfMcm1 was strengthened. Further comparative transcriptome and quantitative PCR analysis revealed that CfMcm1 modulated expression of genes related to conidial development (CfERG5A, CfERG5B, CfHik5, and CfAbaA), appressorium formation (CfCBP1 and CfCHS7), pectin degradation (CfPelA and CfPelB), sexual development (CfMYB, CfFork, CfHMG, and CfMAT1-2-1), and melanin biosynthesis (CfCmr1, CfPKS1, CfT4HR1, CfTHR1, and CfSCD1). Our results demonstrated that CfMcm1 is a pivotal regulator possessing multiple functions in pathogenicity, asexual and sexual reproduction, and melanin biosynthesis.
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