Abstract
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 (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.
Highlights
Botrytis cinerea is a typical necrotrophic plant fungal pathogen that inflicts grey mould on over 1000 plant species (Fillinger and Elad, 2016), including almost all vegetable and fruit crops, and annually causes US$10 billion to US$100 billion in losses worldwide (Weiberg et al, 2013)
We demonstrate that B. cinerea hyphal branching-related factor 1 (BcHbf1) is a novel pathogenicity-associated factor that is only found in B. cinerea genome and is required for conidial morphogenesis, hyphal branching, infection structure development, sclerotial formation and full virulence of the pathogen
To comprehensively understand molecular mechanisms under lying B. cinerea host interactions, we generated a B. cinerea T-DNA insertion mutant library that contains about 50 000 transformants and identified a mutant strain M8008 with a significant reduction in pathogenicity on detached tomato and strawberry leaves from the mutant library
Summary
Botrytis cinerea is a typical necrotrophic plant fungal pathogen that inflicts grey mould on over 1000 plant species (Fillinger and Elad, 2016), including almost all vegetable and fruit crops, and annually causes US$10 billion to US$100 billion in losses worldwide (Weiberg et al, 2013). The main infection source of the pathogen is conidia that germinate on plant surfaces and form appressorium-like structures to facilitate host penetration (Gourgues et al, 2004). B. cinerea induces a very wide range of symptoms; the most typical symptoms on leaves and soft fruits are soft rots, accompanied by collapse and water soaking of parenchyma tissues, followed by a rapid appearance of grey masses of conidia that initiate the round of infection. B. cinerea produces sclerotia that develop within dying host tissues and serve as the long-term survival structures in the life cycle and the primary inoculum in the disease cycle. Sclerotia germinate in early spring to produce conidiophores and multinucleate conidia, serving as a primary source of inoculum (Williamson et al, 2007)
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