Open AccessA novel Botrytis cinerea‐ specific gene BcHBF1 enhances virulence of the grey mould fungus via promoting host penetration and invasive hyphal development
Author(s) -
Liu Yue,
Liu JianeKang,
Li GuiHua,
Zhang MingZhe,
Zhang YingYing,
Wang YuanYuan,
Hou Jie,
Yang Song,
Sun Jiao,
Qin QingMing
Publication year - 2019
Publication title -
molecular plant pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.945
H-Index - 103
eISSN - 1364-3703
pISSN - 1464-6722
DOI - 10.1111/mpp.12788
Subject(s) - appressorium , botrytis cinerea , biology , hypha , virulence , microbiology and biotechnology , mutant , conidiation , pathogen , spore germination , fungus , mycelium , complementation , spore , gene , botany , genetics
Summary 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 ( h yphal b ranching‐related f actor 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.