Abstract
BackgroundNecrotrophic effector proteins secreted by fungal pathogens are important virulence factors that mediate the development of disease in wheat. Pyrenophora tritici-repentis (Ptr), the causal agent of wheat tan spot, has a race structure dependent on the combination of effectors. In Ptr, ToxA and ToxB are known proteinaceous effectors responsible for necrosis and chlorosis respectively. While Ptr ToxA is encoded by the single gene ToxA, ToxB has multiple loci in the Ptr genome, which is postulated to be directly related to the level of ToxB production and leaf chlorosis. Although previous analysis has indicated that the majority of the ToxB loci lie on a single chromosome, the exact number and chromosomal locations for all the ToxB loci have not been fully identified.ResultsIn this study, we have sequenced the genome of a race 5 ToxB-producing isolate (DW5), using PacBio long read technology, and found that ToxB duplications are nested in the complex subtelomeric chromosomal regions. A total of ten identical ToxB gene copies were identified and based on flanking sequence identity, nine loci appeared associated with chromosome 11 and a single copy with chromosome 5. Chromosome 11 multiple ToxB gene loci were separated by large sequence regions between 31 and 66 kb within larger segmental duplications in an alternating pattern related to loci strand, and flanked by transposable elements.ConclusionThis work provides for the first time the full accompaniment of ToxB loci and surrounding regions, and identifies the organization and distribution of ten ToxB loci to subtelomeric regions. To our knowledge, this is the first report of an interwoven strand-related duplication pattern event. This study further highlights the importance of resolving the highly complex distal chromosomal regions, that remain difficult to assemble, and can harbour important effectors and virulence factors.
Highlights
Necrotrophic effector proteins secreted by fungal pathogens are important virulence factors that mediate the development of disease in wheat
The inverse gene-for-gene interactions between host plants and necrotrophic fungal pathogen typically involve pathogen effectors, which interact with a compatible locus in the host leading to toxin sensitivity and disease susceptibility
Pyrenophora tritici-repentis (Ptr) a necrotrophic fungal pathogen and the causal agent of wheat (Triticum aestivum L) tan spot, produces a number of effectors that mediate the development of foliar disease on susceptible wheat genotypes
Summary
Necrotrophic effector proteins secreted by fungal pathogens are important virulence factors that mediate the development of disease in wheat. Pyrenophora tritici-repentis (Ptr) a necrotrophic fungal pathogen and the causal agent of wheat (Triticum aestivum L) tan spot, produces a number of effectors that mediate the development of foliar disease on susceptible wheat genotypes. Tan spot has two distinct leaf symptoms, which are necrosis and chlorosis [1] These symptoms are the result of secreted effectors ToxA, ToxB and ToxC [2,3,4] and other as yet uncharacterised effectors [5, 6]. ToxA and ToxB, are characterised as small effector proteins that produce necrosis and chlorosis symptoms, respectively [2, 4]. While ToxC, which causes chlorosis, has not been characterised and may be the product of a secondary metabolite gene cluster [3]
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