Abstract
Necrotrophic fungi are unable to occupy living plant cells. How such pathogens survive first contact with living host tissue and initiate infection is therefore unclear. Here, we show that the necrotrophic grey mold fungus Botrytis cinerea undergoes massive apoptotic-like programmed cell death (PCD) following germination on the host plant. Manipulation of an anti-apoptotic gene BcBIR1 modified fungal response to PCD-inducing conditions. As a consequence, strains with reduced sensitivity to PCD were hyper virulent, while strains in which PCD was over-stimulated showed reduced pathogenicity. Similarly, reduced levels of PCD in the fungus were recorded following infection of Arabidopsis mutants that show enhanced susceptibility to B. cinerea. When considered together, these results suggest that Botrytis PCD machinery is targeted by plant defense molecules, and that the fungal anti-apoptotic machinery is essential for overcoming this host-induced PCD and hence, for establishment of infection. As such, fungal PCD machinery represents a novel target for fungicides and antifungal drugs.
Highlights
Plant pathogenic fungi have evolved two prominent infection strategies: biotrophic pathogens proliferate within the living plant tissue deriving nutrition from living plant cells, and necrotrophic pathogens that do not occupy living plant cells and instead, kill host cells before tissue colonization
Our work provides a fundamental new insight into the biology and infection strategy of Botrytis cinerea, an economically important plant pathogen, which is used as a model for studying pathogenicity of necrotrophic plant pathogens
A fundamental question that we sought to address in this study is how B. cinerea, and possibly other necrotrophic pathogens, overcome the plant defenses in living host cells
Summary
Plant pathogenic fungi have evolved two prominent infection strategies: biotrophic pathogens proliferate within the living plant tissue deriving nutrition from living plant cells, and necrotrophic pathogens that do not occupy living plant cells and instead, kill host cells before tissue colonization. Necrotrophic pathogens secrete enzymes and toxins that kill the host tissue ahead of pathogen invasion, avoiding direct contact with defense molecules in living plant cells. It is unclear how this group of pathogens overcomes the host defenses during the early stages of infection, when the fungus is in contact with living host cells. The plant defense responses activated by B. cinerea are regulated in several ways, including the jasmonate and ethylene signaling pathways, as well as by additional signaling cascades that have not yet been identified [7,8,9]. These defense responses can slow B. cinerea infection, but they do not completely block disease development [10,11,12]
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