Rust fungi cause devastating diseases of wheat and other cereal species globally. Genetic resistance is the preferred method to control rusts but the effectiveness of race-specific resistance is typically transient due to the genetic plasticity of rust populations. The advent of RNA interference (RNAi) technology has shown promise for the engineering of resistance to some biotrophic pathogens in plants by altering the expression of essential pathogens' genes. Gene fragments from the rust fungi Puccinia striiformis f. sp. tritici or P. graminis f. sp. tritici were delivered to plant cells through the Barley stripe mosaic virus system, and some reduced the expression of the corresponding genes in the rust fungus. The ability to detect suppression was associated with the expression patterns of the fungal genes because reduction was only detected in transcripts with relatively high levels of expression in fungal haustoria. The results indicate that an in planta RNAi approach can be used in functional genomics research for rust fungi and that it could potentially be used to engineer durable resistance.
Gibberella zeae is the major fungal pathogen of Fusarium head blight of wheat and produces several mycotoxins that are harmful to humans and domesticated animals. We identified loci associated with pathogenicity and aggressiveness on an amplified fragment length polymorphism based genetic map of G. zeae in a cross between a lineage 6 nivalenol producer from Japan and a lineage 7 deoxynivalenol producer from Kansas. Ninety-nine progeny and the parents were tested in the greenhouse for 2 years. Progeny segregated qualitatively (61:38) for pathogenicity:nonpathogenicity, respectively. The trait maps to linkage group IV, which is adjacent to loci that affect colony pigmentation, perithecium production, and trichothecene toxin amount. Among the 61 pathogenic progeny, the amount of disease induced (aggressiveness) varied quantitatively. Two reproducible quantitative trait loci (QTL) for aggressiveness were detected on linkage group I using simple interval analysis. A QTL linked to the TRI5 locus (trichodiene synthase in the trichothecene pathway gene cluster) explained 51% of the variation observed, and a second QTL that was 50 centimorgans away explained 29% of the phenotypic variation. TRI5 is tightly linked to the locus controlling trichothecene toxin type. The two QTLs, however, were likely part of the same QTL using composite interval analysis. Progeny that produced deoxynivalenol were, on average, approximately twice as aggressive as those that produced nivalenol. No transgressive segregation for aggressiveness was detected. The rather simple inheritance of both traits in this interlineage cross suggests that relatively few loci for pathogenicity or aggressiveness differ between lineage 6 and 7.
Gibberella moniliformis (Fusarium verticillioides) is primarily a pathogen of maize, but it can also cause disease in other crop species. This pathogenicity, as well as the contamination of food-and feedstuffs with the fumonisin mycotoxins, results in economically significant losses to both farmers and food processors. The dissection of important biological characters in this fungus has been hampered by the lack of a uniformly dense genetic map. The existing restriction fragment length polymorphism-based map contains significant gaps, making it difficult to routinely locate biologically important genes, such as those involved in pathogenicity or mycotoxin production, with precision. We utilized amplified fragment length polymorphisms (AFLPs) to saturate the existing genetic map and added 486 AFLP markers to the ϳ150 markers on the existing map. The resulting map has an average marker interval of 3.9 map units and averages ϳ21 kb/map unit. The additional markers expanded the map from 1,452 to 2,188 map units distributed across 12 chromosomes. The maximum distance between adjacent markers is 29 map units. We identified AFLP markers less than 1 map unit from the mating type (MAT) locus and 2.5 map units from the spore killer (SK) locus; eight AFLP markers map within 8.5 units of the FUM1 (fumonisin biosynthetic) locus. The increased saturation of this map will facilitate further development of G. moniliformis as a model system for the genetic and population genetic studies of related, but less genetically tractable, plant pathogenic fungi.Gibberella moniliformis Wineland [anamorph Fusarium verticillioides (Sacc.) Nirenberg] is genetically the most intensively studied species in Fusarium section Liseola. A number of morphological and physiological mutants have been characterized in addition to anonymous restriction fragment length polymorphism (RFLP) markers (3,23,25,37,38,47
In the fungus Fusarium sporotrichioides, biosynthesis of trichothecene mycotoxins requires at least three genetic loci: a core 12-gene cluster, a smaller two-gene cluster, and a single-gene locus. Here, we describe the Tri15 gene, which represents a fourth locus involved in trichothecene biosynthesis. Tri15 is predicted to encode a Cys(2)-His(2 )zinc finger protein and is expressed in a manner similar to genes in the core trichothecene gene cluster. However, disruption of F. sporotrichioides Tri15 does not affect production of T-2 toxin, the major trichothecene produced by this fungus. This result suggests that Tri15 is not necessary for the production of toxin. Cultures with exogenously added T-2 toxin have high levels of Tri15 expression and no detectable expression of the trichothecene biosynthetic genes Tri5 and Tri6. The expression analysis is consistent with Tri15 being a negative regulator of at least some of the trichothecene biosynthetic genes. In F. graminearum, Tri15 has been mapped to linkage group 2 and is therefore unlinked to the main trichothecene biosynthetic gene cluster.
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