Activation of a wheat gene product by a fungal protein leads to cell death in the plant, allowing the pathogen to cause disease.
BackgroundPyrenophora tritici-repentis (Ptr) is a necrotrophic fungal pathogen that causes the major wheat disease, tan spot. We set out to provide essential genomics-based resources in order to better understand the pathogenicity mechanisms of this important pathogen.ResultsHere, we present eight new Ptr isolate genomes, assembled and annotated; representing races 1, 2 and 5, and a new race. We report a high quality Ptr reference genome, sequenced by PacBio technology with Illumina paired-end data support and optical mapping. An estimated 98% of the genome coverage was mapped to 10 chromosomal groups, using a two-enzyme hybrid approach. The final reference genome was 40.9 Mb and contained a total of 13,797 annotated genes, supported by transcriptomic and proteogenomics data sets.ConclusionsWhole genome comparative analysis revealed major chromosomal segmental rearrangements and fusions, highlighting intraspecific genome plasticity in this species. Furthermore, the Ptr race classification was not supported at the whole genome level, as phylogenetic analysis did not cluster the ToxA producing isolates. This expansion of available Ptr genomics resources will directly facilitate research aimed at controlling tan spot disease.Electronic supplementary materialThe online version of this article (10.1186/s12864-018-4680-3) contains supplementary material, which is available to authorized users.
SUMMARYThe pathogen Stagonospora nodorum produces multiple effectors, also known as host-selective toxins (HSTs), that interact with corresponding host sensitivity genes in an inverse gene-for-gene manner to cause the disease Stagonospora nodorum blotch (SNB) in wheat. In this study, a sensitivity gene was identified in Aegilops tauschii, the diploid D-genome donor of common wheat. The gene was mapped to the short arm of chromosome 5D and mediated recognition of the effector SnTox3, which was previously shown to be recognized by the wheat gene Snn3 on chromosome arm 5BS. Comparative mapping suggested that Snn3 and the gene on 5DS are probably homoeologous and derived from a common ancestor. Therefore, we propose to designate these genes as Snn3-B1 and Snn3-D1, respectively. Compatible Snn3-D1-SnTox3 interactions resulted in more severe necrosis in both effector infiltration and spore inoculation experiments than compatible Snn3-B1-SnTox3 interactions, indicating that Snn3-B1 and Snn3-D1 may have different affinities in SnTox3 recognition or signal transduction. Wheat bin-mapped expressed sequence tags and good levels of collinearity among the wheat Snn3 regions, rice (Oryza sativa), and Brachypodium distachyon were exploited for saturation and fine mapping of the Snn3-D1 locus. Markers delineating the Snn3-D1 locus to a 1.4 cM interval will be useful for initiating positional cloning. Further characterization of how these homoeologous genes mediate recognition of the same pathogen effector should enhance understanding of host manipulation by necrotrophic pathogens in causing disease.
Parastagonospora (syn. ana, Stagonospora; teleo, Phaeosphaeria) nodorum (Berk.) Quaedvleig, Verkley & Crous is a necrotrophic fungal pathogen that causes the disease Septoria nodorum blotch (SNB) on wheat (Triticum aestivum L. subsp. aestivum). The fungus produces necrotrophic effectors (NEs) that cause cell death when recognized by corresponding host genes, which ultimately leads to disease. To date, eight host gene-NE interactions have been described in the wheat-P. nodorum system. Here, we report the identification and partial characterization of a ninth interaction involving a P. nodorum-produced NE designated SnTox7 and a wheat gene designated Snn7. SnTox7 is a small protein with an estimated size less than 30 kDa and largely resistant to heat and chemical treatment. The Snn7 gene governs sensitivity to SnTox7 and was delineated to a 2.7-cM interval on the long arm of wheat chromosome 2D. The Snn7-SnTox7 interaction explained 33% of the variation in disease among a segregating population, indicating that the interaction plays a prominent role in the development of SNB. The Snn7 sensitivity allele was identified in the hexaploid wheat cultivar Timstein, but evaluation of a set of 52 hexaploid lines of diverse origin indicated that few genotypes harbored a functional Snn7 allele, thus indicating that Snn7 is relatively rare. The identification of the Snn7-SnTox7 interaction adds to our knowledge of the wheat-P. nodorum pathosystem, which has become a model for necrotrophic specialist fungal pathogens and their interactions with plants leading to necrotrophic effector-triggered susceptibility.
Although the impacts of crop domestication on specialist pathogens are well known, less is known about the interaction of crop variation and generalist pathogens. To study how genetic variation within a crop affects plant resistance to generalist pathogens, we infected a collection of wild and domesticated tomato accessions with a genetically diverse population of the generalist pathogen Botrytis cinerea. We quantified variation in lesion size of 97 B. cinerea genotypes (isolates) on six domesticated tomato genotypes (Solanum lycopersicum) and six wild tomato genotypes (Solanum pimpinellifolium). Lesion size was significantly affected by large effects of the host and pathogen's genotype, with a much smaller contribution of domestication. This pathogen collection also enables genome-wide association mapping of B. cinerea. Genome-wide association mapping of the pathogen showed that virulence is highly polygenic and involves a diversity of mechanisms. Breeding against this pathogen would likely require the use of diverse isolates to capture all possible mechanisms. Critically, we identified a subset of B. cinerea genes where allelic variation was linked to altered virulence against wild versus domesticated tomato, as well as loci that could handle both groups. This generalist pathogen already has a large collection of allelic variation that must be considered when designing a breeding program.
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