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The plant-pathogenic fungus Mycosphaerella graminicola (asexual stage: Septoria tritici) causes septoria tritici blotch, a disease that greatly reduces the yield and quality of wheat. This disease is economically important in most wheat-growing areas worldwide and threatens global food production. Control of the disease has been hampered by a limited understanding of the genetic and biochemical bases of pathogenicity, including mechanisms of infection and of resistance in the host. Unlike most other plant pathogens, M. graminicola has a long latent period during which it evades host defenses. Although this type of stealth pathogenicity occurs commonly in Mycosphaerella and other Dothideomycetes, the largest class of plant-pathogenic fungi, its genetic basis is not known. To address this problem, the genome of M. graminicola was sequenced completely. The finished genome contains 21 chromosomes, eight of which could be lost with no visible effect on the fungus and thus are dispensable. This eight-chromosome dispensome is dynamic in field and progeny isolates, is different from the core genome in gene and repeat content, and appears to have originated by ancient horizontal transfer from an unknown donor. Synteny plots of the M. graminicola chromosomes versus those of the only other sequenced Dothideomycete, Stagonospora nodorum, revealed conservation of gene content but not order or orientation, suggesting a high rate of intra-chromosomal rearrangement in one or both species. This observed "mesosynteny" is very different from synteny seen between other organisms. A surprising feature of the M. graminicola genome compared to other sequenced plant pathogens was that it contained very few genes for enzymes that break down plant cell walls, which was more similar to endophytes than to pathogens. The stealth pathogenesis of M. graminicola probably involves degradation of proteins rather than carbohydrates to evade host defenses during the biotrophic stage of infection and may have evolved from endophytic ancestors.

Charcoal rot of soybean [Glycine max (L.) Merr.], caused by the soilborne fungus Macrophomina phaseolina (Tassi) Goid., has ranked among the most important soybean diseases in the United States. Disease management is typically done in a multifaceted approach through crop rotation, tillage, irrigation, and seed treatments aimed at minimizing damage caused by the pathogen. Development of genetic resistance to charcoal rot appears to be the most efficient strategy to control the disease; however, there are no reports of genetic regions associated with resistance to the disease. The objective of this study was to identify quantitative trait loci (QTLs) governing resistance to charcoal rot in soybean using a biparental population of PI 567562A (resistant) × PI 567437 (susceptible). A total of 140 F2–derived lines were genotyped with 5403 single nucleotide polymorphism (SNP) markers covering 20 chromosomes, of which 2283 were polymorphic. Resistance to charcoal rot was evaluated in the F2:3 lines using the cut‐stem inoculation technique under greenhouse conditions. The QTL mapping analysis indicated one QTL on chromosome 15 explaining 29.4% of phenotypic variation, and two QTLs on chromosome 16 explaining 25.4 and 8.4% of phenotypic variation for resistance to M. phaseliona. To our knowledge, this is the first report of genomic regions harboring resistance to charcoal rot in soybean, and it may facilitate breeding and molecular engineering progress to combat charcoal rot disease in the future. [ABSTRACT FROM AUTHOR]