The Leotiomycete Botrytis cinerea is a high-impact plant pathogen causing gray mold disease in a wide range of dicotyledonous species. Besides its efficient strategies to cause disease - either by being highly aggressive leading to rapid destruction of plant tissues or by keeping hidden for certain periods before damaging the host - the fungus is well-adapted to the changing environmental conditions due to different modes of reproduction for dispersal (macroconidia), survival (sclerotia) or adaptation (ascospores formed in the apothecia). The screening of a collection of B. cinerea mutants generated by Agrobacterium tumefaciens-mediated transformation (ATMT) has revealed a number of virulence-attenuated mutants. In the avirulent mutant PA2810 the inserted T-DNA disrupts the gene encoding a putative histone 3 lysine 36 (H3K36)-specific demethylase (BcKDM1). Targeted mutagenesis of bckdm1 confirmed the gene-phenotype linkage and indicated that BcKDM1, despite its role in virulence (critical for penetration), is required for coping with excessive light, oxidative stress and for proper expression of light-responsive genes and photomorphogenesis. Thus, bckdm1 loss-of-function mutants produce sclerotia under unfavorable conditions such as in the light. Notably, mutants expressing a truncated BcKDM1 (bckdm1991aa) showed deviating phenotypes from deletion (Δbckdm1) and demethylase-deficient (bckdm1H360A) mutants but also from the wild type, thereby indicating the importance of the C-terminal region for some developmental processes. This effect may be specific to B. cinerea as the orthologs from other Ascomycetes cannot replace BcKDM1.
Keywords: Botrytis cinerea; Development; Forward genetics; Histone demethylase; Light; Virulence.
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