Disease resistance. Insensitivity to the toxins produced by Pyrenophora tritici-repentis and Stagonospora nodorum.

Tsn1

1. Chromosomal location of a gene conditioning insensitivity in wheat to a necrosis-inducing culture filtrate from Pyrenophora tritici-repentis. Faris JD, Anderson JA, Francl LJ, Jordahl JG. In: Phytopathology, 1996, 86: 459-463.

Previous research indicates that infection by the tan spot fungus (Pyrenophora tritici-repentis) produces two genetically distinct symptoms in wheat (Triticum aestivum): tan necrosis and extensive chlorosis. Necrosis-inducing isolates of P. tritici-repentis release a host-selective toxin in culture that produces a reaction highly associated with the induction of tan necrosis in susceptible wheat genotypes. The objectives of this research were to determine the number of genes conditioning insensitivity to a necrosis-inducing culture filtrate in a population of wheat F₃ families, and to map the insensitivity gene(s) using restriction fragment length polymorphisms (RFLPs). The population consisted of 58 F₃ families derived from the cross of a resistant synthetic hexaploid, W-7976, with the susceptible cultivar 'Kulm.' At least 16 individuals from each F₃ family were infiltrated with culture filtrate from the P. tritici-repentis isolate 86-124 and were scored as insensitive or sensitive. Low-copy DNA clones that hybridized to group 5 wheat chromosomes were used to detect RFLPs associated with insensitivity. The families segregated in a ratio of 15:29:14 homozygous insensitive/segregating/homozygous sensitive, suggesting that a single nuclear gene was responsible for conditioning insensitivity to the pathogenic factor(s) in the culture filtrate. RFLPs were detected that flanked the locus conferring insensitivity at distances of 5.7 and 16.5 cM. Aneuploid analysis indicated that this gene resided on the long arm of chromosome 5B. We proposed the symbol tsn1 to designate this gene.

2. Host-parasite interaction in tan spot (Pyrenophora tritici-repentis) of wheat. Strelkov SE, Lamari L In: Canadian Journal of Plant Pathology, 2003, 25: 339-349.

Tan spot of wheat, caused by the ascomycete Pyrenophora tritici-repentis, is an economically important disease in all the major wheat growing areas worldwide. Even though the pathogen was known to occur on grasses and episodically on wheat for more than eight decades, large-scale epidemics of tan spot were first recorded in the early 1970s. The increased incidence was associated with stubble retention, a practice implemented in the context of soil conservation. The present review highlights some of the recent developments that have occurred in studies of the wheat - P. tritici-repentis interaction and discusses the implications for our understanding of host-parasite relations in general. Races of P. tritici-repentis produce at least three host-specific toxins, effective on particular host lines or cultivars. Single dominant and independently inherited genes control host reaction to these toxins, with one gene for each toxin. Eight races of the pathogen have now been identified from collections made in several parts of the world, accounting for all virulence patterns expected from three toxins matching three "susceptibility" genes in the host. Genetic analyses of host and pathogen suggested that a one-to-one relationship existed in the wheat - P. tritici-repentis interaction. The model described for tan spot of wheat appears to be a mirror image of the classical gene-for-gene in that it is based on compatibility. Thus, it is proposed that the gene-for-gene model can be extended, as previously predicted by others, to pathosystems involving multiple host-specific toxins. The relationship between toxin production and the evolution of new races is also discussed.

3. Identification of quantitative trait loci for race-nonspecific resistance to tan spot of wheat. Faris JD, Friesen TL In: Theoretical and Applied Genetics, 2005, 111: 386-392.

Tan spot, caused by Pyrenophora tritici-repentis (Ptr), is an economically important foliar disease in the major wheat growing areas throughout the world. Multiple races of the pathogen have been characterized based on their ability to cause necrosis and/or chlorosis on differential wheat lines. In this research, we evaluated a population of recombinant inbred lines derived from a cross between the common wheat varieties Grandin and BR34 for reaction to tan spot caused by Ptr races 1-3 and 5. Composite interval mapping revealed QTLs on the short arm of chromosome 1B and the long arm of chromosome 3B that were significantly associated with resistance to all four races. The effects of the two QTLs varied for the different races. The 1B QTL explained from 13% to 29% of the phenotypic variation, whereas the 3B QTL explained from 13% to 41% of the variation. Additional minor QTLs were detected but not associated with resistance to all races. The host-selective toxin Ptr ToxA, which is produced by races 1 and 2, was not a significant factor in the development of disease in this population. The race-nonspecific resistance derived from BR34 may take precedence over the gene-for-gene interaction known to be associated with the wheat-Ptr system.

4. Role of host sensitivity to Ptr ToxA in development of tan spot of wheat. Friesen TL, Ali S, Kianian S, Francl LJ, Rasmussen JB In: Phytopathology, 2003, 93: 397-401.

Pyrenophora tritici-repentis race 2 produces Ptr ToxA, a host-selective toxin previously described as a pathogenicity factor for tan spot on wheat. The objective of this research was to evaluate the role of host sensitivity to toxin, conditioned by a single dominant gene on chromosome 5BL, in the disease development by race 2. An F-derived F₆ recombinant inbred population of 108 wheat lines, produced from crosses of toxin-sensitive, disease-susceptible cv. Kulm with the toxin-insensitive, disease-resistant cv. Erik segregated 1: 1 for toxin reaction. However, the population was skewed toward resistance to race 2 of the fungus. Toxin reaction accounted for 24.4% of the genetic variance for disease. Heritability estimates suggested the presence of four to five genes that influence disease reaction in the population. Toxin-insensitive mutants, previously derived Kulm, were susceptible to race 2, although disease developed more slowly on the mutants than it did on the wildtype Kuhn. The data indicate that sensitivity to Ptr ToxA influences disease severity in some host genotypes without defining susceptibility.

5. Genomic targeting and high-resolution mapping of the Tsn1 gene in wheat. Haen KM, Lu HJ, Friesen TL, Faris JD In: Crop Science, 2004, 44: 951-962.

Tan spot, caused by the fungal pathogen Pyrenophora tritici-repentis (Died.) Drechs. causes severe yield losses in wheat (Triticum aestivum L., 2n = 6x = 42, AABBDD) and durum (T. turgidum L., 2n = 4x = 28, AABB). The Tsn1 gene acts dominantly to confer sensitivity to a host-selective proteinaceous toxin (Ptr ToxA) produced by the fungus. Our objectives were to: (i) target markers to the Tsn1 genomic region and (ii) develop a high-resolution map of the Tsn1 locus. The techniques of methylation-sensitive AFLP, traditional AFLP, and cDNA-AFLP were combined with bulked segregant analysis (BSA) using various wheat and durum cytogenetic stocks to target markers to the Tsn1 genomic region. Over 500 primer combinations were screened resulting in the identification of 18 low-copy markers closely linked to Tsn1. High-resolution mapping of the markers delineated the Tsn1 gene to a 0.2 cM interval in a hexaploid wheat population consisting of 1266 gametes, and to 0.8 cM in a durum wheat population consisting of 1860 gametes. Comparisons with rice BAC/PAC sequences indicated the lack of colinearity within the Tsn1 genomic region. Tsn1 was located within a gene-rich recombination hot spot region, and the physical distance separating the flanking markers may be as little as 200 kb. Therefore, these markers will serve as a basis for the map-based cloning of Tsn1. The isolation of Tsn1 will further our knowledge of wheat-tan spot interactions as well as host-pathogen interactions in general.