College of Plant Sciences, Key Laboratory of Zoonosis Research, Ministry of Education, Jilin University, Changchun, 130062, China.
College of Plant Sciences, Jilin University, Changchun, 130062, China.
Mol Plant Pathol. 2019 May;20(5):731-747. doi: 10.1111/mpp.12788.
Botrytis cinerea is the causative agent of grey mould on over 1000 plant species and annually causes enormous economic losses worldwide. However, the fungal factors that mediate pathogenesis of the pathogen remain largely unknown. Here, we demonstrate that a novel B. cinerea-specific pathogenicity-associated factor BcHBF1 (hyphal branching-related factor 1), identified from virulence-attenuated mutant M8008 from a B. cinerea T-DNA insertion mutant library, plays an important role in hyphal branching, infection structure formation, sclerotial formation and full virulence of the pathogen. Deletion of BcHBF1 in B. cinerea did not impair radial growth of mycelia, conidiation, conidial germination, osmotic- and oxidative-stress adaptation, as well as cell wall integrity of the ∆Bchbf1 mutant strains. However, loss of BcHBF1 impaired the capability of hyphal branching, appressorium and infection cushion formation, appressorium host penetration and virulence of the pathogen. Moreover, disruption of BcHBF1 altered conidial morphology and dramatically impaired sclerotial formation of the mutant strains. Complementation of BcHBF1 completely rescued all the phenotypic defects of the ∆Bchbf1 mutants. During young hyphal branching, host penetration and early invasive growth of the pathogen, BcHBF1 expression was up-regulated, suggesting that BcHBF1 is required for these processes. Our findings provide novel insights into the fungal factor mediating pathogenesis of the grey mould fungus via regulation of its infection structure formation, host penetration and invasive hyphal branching and growth.
灰葡萄孢是 1000 多种植物物种上灰霉病的病原体,每年在全球范围内造成巨大的经济损失。然而,介导病原菌发病机制的真菌因子在很大程度上仍然未知。在这里,我们证明了一种新的灰葡萄孢特异性致病性相关因子 BcHBF1(菌丝分支相关因子 1),它是从灰葡萄孢 T-DNA 插入突变体文库中的致病力减弱突变体 M8008 中鉴定出来的,在菌丝分支、侵染结构形成、菌核形成和病原菌的完全毒力中起着重要作用。在灰葡萄孢中删除 BcHBF1 不会损害菌丝的径向生长、分生孢子形成、分生孢子萌发、渗透和氧化应激适应以及∆Bchbf1 突变菌株的细胞壁完整性。然而,BcHBF1 的缺失削弱了菌丝分支、附着胞和侵染垫形成、附着胞宿主穿透和病原菌的毒力的能力。此外,BcHBF1 的破坏改变了分生孢子的形态,并严重削弱了突变菌株的菌核形成。BcHBF1 的互补完全挽救了∆Bchbf1 突变体的所有表型缺陷。在年轻的菌丝分支、宿主穿透和病原菌的早期侵袭生长过程中,BcHBF1 的表达被上调,表明 BcHBF1 是这些过程所必需的。我们的研究结果为通过调节其侵染结构形成、宿主穿透和侵袭性菌丝分支和生长来介导灰霉菌发病机制的真菌因子提供了新的见解。