Inheritance and interaction of spring wheat (Triticum aestivum L.) resistance to Race 2 and Race 3 of Pyrenophora tritici-repentis (Died.) Drechs.

2001 ◽  
Vol 81 (3) ◽  
pp. 527-533 ◽  
Author(s):  
S. D. Duguid ◽  
A. L. Brûlé-Babel
Keyword(s):  
Triticum Aestivum ◽  
Fungal Pathogen ◽  
Nuclear Gene ◽  
Triticum Aestivum L ◽  
Tan Spot ◽  
Pyrenophora Tritici Repentis ◽  
Ptr Toxa ◽  
Recessive Genes ◽  
Race 2 ◽  
Dominant Genes

Tan spot is a residue-borne leaf spotting disease caused by the fungal pathogen Pyrenophora tritici-repentis. An understanding of the inheritance of resistance is required to build a strategy for incorporating tan spot resistance into commercial cultivars of wheat. The objectives of this study were to determine the inheritance of host resistance to isolates of races 2 (a necrosis-inducing race) and 3 (a chlorosis-inducing race) of P. tritici-repentis. Crosses were made between seven wheat (Triticum aestivum) genotypes (Katepwa, BH1146, ST15, ST6, Erik, 6B1043, 6B367). Parents, F1, F2and F2-derived F3 populations were inoculated with isolates 86-124 and D308 (races 2 and 3, respectively) of P. tritici-repentis and infiltrated with Ptr ToxA. Resistance to 86-124 and insensitivity to Ptr ToxA was controlled by a single recessive nuclear gene in all of the resistant/susceptible crosses. In contrast, resistance to D308 was controlled by a single dominant nuclear gene in five crosses and two genes in two crosses. In the BH1146/ST15 cross two dominant genes controlled resistance to D308, while in the Katepwa/ST15 cross two recessive genes controlled resistance. Reactions to race 2 were independent of reactions to race 3 and controlled by independent genetic systems. Key words: Triticum aestivum L., Pyrenophora tritici-repentis (Died.) Drechs., disease resistance, inheritance, Ptr necrosis toxin, tan spot

scholarly journals Characterizing Virulence of the Pyrenophora tritici-repentis Isolates Lacking Both ToxA and ToxB Genes

Pathogens ◽  
2018 ◽  
Vol 7 (3) ◽  
pp. 74 ◽  
Author(s):  
Jingwei Guo ◽  
Gongjun Shi ◽  
Zhaohui Liu
Keyword(s):  
Triticum Aestivum L ◽  
Tan Spot ◽  
Pyrenophora Tritici Repentis ◽  
Tan Spot Disease ◽  
Hard Red Winter Wheat ◽  
Winter Wheat Cultivars ◽  
Race 2 ◽  
Genomic Regions ◽  
Race 4 ◽  
Necrotrophic Effectors

The fungus Pyrenophora tritici-repentis (Ptr) causes tan spot of wheat crops, which is an important disease worldwide. Based on the production of the three known necrotrophic effectors (NEs), the fungal isolates are classified into eight races with race 4 producing no known NEs. From a laboratory cross between 86–124 (race 2 carrying the ToxA gene for the production of Ptr ToxA) and DW5 (race 5 carrying the ToxB gene for the production of Ptr ToxB), we have obtained some Ptr isolates lacking both the ToxA and ToxB genes, which, by definition, should be classified as race 4. In this work, we characterized virulence of two of these isolates called B16 and B17 by inoculating them onto various common wheat (Triticum aestivum L.) and durum (T. turgidum L.) genotypes. It was found that the two isolates still caused disease on some genotypes of both common and durum wheat. Disease evaluations were also conducted in recombinant inbred line populations derived from two hard red winter wheat cultivars: Harry and Wesley. QTL mapping in this population revealed that three genomic regions were significantly associated with disease, which are different from the three known NE sensitivity loci. This result further indicates the existence of other NE-host sensitivity gene interactions in the wheat tan spot disease system.

A gene for resistance to a necrosis-inducing isolate of Pyrenophora tritici-repentis located on 5BL of Triticum aestivum cv. Chinese Spring

Genome ◽  
1996 ◽  
Vol 39 (3) ◽  
pp. 598-604 ◽  
Author(s):  
W. S. Stock ◽  
A. L. Brûlé-Babel ◽  
G. A. Penner
Keyword(s):  
Triticum Aestivum ◽  
Resistance Gene ◽  
Chinese Spring ◽  
Recessive Gene ◽  
Triticum Aestivum L ◽  
Tan Spot ◽  
Monosomic Analysis ◽  
Chromosome Location ◽  
Pyrenophora Tritici Repentis ◽  
Chromosome Arm

Several sources of high-level resistance to tan spot caused by Pyrenophora tritici-repentis have been identified in hexaploid wheat (Triticum aestivum L.). This study was conducted to determine the number and chromosome location of a gene(s) in the cultivar Chinese Spring (CS) that confers resistance to a tan necrosis inducing isolate (nec+chl−) of P. tritici-repentis, 86-124, and insensitivity to Ptr necrosis toxin. Reciprocal crosses were made between CS (resistant–insensitive) and 'Kenya Farmer' (KF) (susceptible–sensitive). Analysis of the CS/KF F1and F2 populations and F2-derived F3 families identified a single nuclear recessive gene governing resistance to isolate 86-124 and Ptr necrosis toxin. Evaluation of the CS(KF) substitution series, F2 monosomic analysis, and screening of a series of 19 CS compensating nullitetrasomic and two ditelosomic lines (2AS and 5BL) indicated that the resistance gene was located on chromosome arm 5BL. No linkage exists between Lr18 and the tan necrosis resistance gene on chromosome arm 5BL. It is proposed that the gene for resistance to the tan necrosis inducing isolate 86-124 (nec+chl−) of P. tritici-repentis and Ptr necrosis toxin be named tsn1. Key words : wheat, Triticum aestivum L., tan spot resistance, Pyrenophora tritici-repentis (Died.) Drechs., chromosome location, Ptr necrosis toxin.

scholarly journals Role of Host Sensitivity to Ptr ToxA in Development of Tan Spot of Wheat

2003 ◽  
Vol 93 (4) ◽  
pp. 397-401 ◽  
Author(s):  
T. L. Friesen ◽  
S. Ali ◽  
S. Kianian ◽  
L. J. Francl ◽  
J. B. Rasmussen
Keyword(s):  
Genetic Variance ◽  
Dominant Gene ◽  
Tan Spot ◽  
Wild Type ◽  
Pyrenophora Tritici Repentis ◽  
Ptr Toxa ◽  
Recombinant Inbred Population ◽  
Race 2 ◽  
Wheat Lines

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 F2-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 wild-type Kulm. The data indicate that sensitivity to Ptr ToxA influences disease severity in some host genotypes without defining susceptibility.

Inheritance of resistance to a necrosis- and chlorosis-inducing isolate from Race 1 of Pyrenophora tritici-repentis in spring wheat

2001 ◽  
Vol 81 (3) ◽  
pp. 519-525 ◽  
Author(s):  
S. D. Duguid ◽  
A. L. Brûlé-Babel
Keyword(s):  
Triticum Aestivum ◽  
Conservation Tillage ◽  
Dominant Gene ◽  
Recessive Gene ◽  
Tan Spot ◽  
Inheritance Of Resistance ◽  
Pyrenophora Tritici Repentis ◽  
Ptr Toxa ◽  
Race 1 ◽  
Resistant Genotypes

Tan spot is a stubble-borne foliar disease of wheat (Triticum aestivum L.) caused by Pyrenophora tritici-repentis (Died.) Drechs. The potential for yield losses due to tan spot has increased with the adoption of conservation tillage practices. The main objective of this study was to determine the inheritance of resistance among seven wheat genotypes to the tan necrosis- and chlorosis-in ducing, race 1, isolate ASC1 (nec+ chl+), and the necrosis-inducing toxin, Ptr ToxA. Crosses were made between four resistant (Erik, ST6, 6B367, 6B1043) and three susceptible genotypes (Katepwa, BH1146, ST15). Parental, F1 and F2 populations were inoculated with ASC1 and infiltrated with Ptr ToxA under controlled environments. F2-derived F3 families were grown in the field and inoculated with ASC1. No reciprocal differences were observed. Resistance to the tan necrosis-inducing component of ASC1 and insensitivity to Ptr ToxA was controlled by a single recessive gene, whereas resistance to the chlorosis-inducing component of ASC1 was controlled by a single dominant gene. Genetic control of responses to each component (tan necrosis- or chlorosis-inducing) of ASC1 was independent. Lack of segregation among F2 progeny from crosses between resistant genotypes indicated that resistant genotypes carry at least one gene in common for resistance to ASC1. Key words: Triticum aestivum, Pyrenophora tritici-repentis, disease resistance, inheritance, Ptr ToxA, necrosis, chlorosis, toxin, tan spot, leaf spot

scholarly journals A Combination of Phenotypic and Genotypic Characterization Strengthens Pyrenophora tritici-repentis Race Identification

2007 ◽  
Vol 97 (6) ◽  
pp. 694-701 ◽  
Author(s):  
Rachael M. Andrie ◽  
Iovanna Pandelova ◽  
Lynda M. Ciuffetti
Keyword(s):  
Visual Assessment ◽  
Tan Spot ◽  
Disease Phenotypes ◽  
Pyrenophora Tritici Repentis ◽  
Ptr Toxa ◽  
Differential Set ◽  
Standard Set ◽  
Race 2 ◽  
Unique Specificity ◽  
Cultivar Specificity

Pyrenophora tritici-repentis, causal agent of tan spot of wheat, produces multiple host-selective toxins (HSTs), including Ptr ToxA, Ptr ToxB, and Ptr ToxC. The specific complement of HSTs produced by a particular isolate determines its host cultivar specificity. Each unique specificity profile, represented by the differential induction of necrosis or chlorosis on a standard set of wheat differentials, defines a unique race. Eight races of P. tritici-repentis have been formally published, although additional races are under investigation. Although visual assessment of disease phenotype is often used in race designation of P. tritici-repentis, our results suggest that it has the potential to be misleading. Inoculation of the P. tritici-repentis isolates SO3 and PT82 on the current wheat differential set indicated classification as race 2 and race 8, respectively; however, genetic characterization revealed that these isolates do not possess the associated HSTs expected for these race assignments. Despite sharing disease phenotypes similar to known races, SO3 and PT82 were genotypically distinct from these previously characterized races of P. tritici-repentis. To ensure detection of the breadth of physiological variation among the isolates of P. tritici-repentis, our results indicate that race classification, where possible, should include both phenotypic and genotypic analyses and eventual expansion of the differential set.

Tan spot of wheat (Triticum aestivum L.) infection at different stages of crop development and inoculum type

2003 ◽  
Vol 22 (1) ◽  
pp. 157-169 ◽  
Author(s):  
Analı́a Perello ◽  
Virginia Moreno ◽  
Marı́a Rosa Simón ◽  
Marina Sisterna
Keyword(s):  
Triticum Aestivum ◽  
Triticum Aestivum L ◽  
Tan Spot ◽  
Crop Development ◽  
Inoculum Type

scholarly journals A Novel Source of Resistance in Wheat to Pyrenophora tritici-repentis Race 1

Plant Disease ◽  
2008 ◽  
Vol 92 (1) ◽  
pp. 91-95 ◽  
Author(s):  
Sukhwinder Singh ◽  
William W. Bockus ◽  
Indu Sharma ◽  
Robert L. Bowden
Keyword(s):  
Great Plains ◽  
Recombinant Inbred Lines ◽  
The United States ◽  
Interval Mapping ◽  
Tan Spot ◽  
Sources Of Resistance ◽  
Pyrenophora Tritici Repentis ◽  
Ptr Toxa ◽  
Chromosome 5B ◽  
Race 1

Tan spot, caused by the fungus Pyrenophora tritici-repentis, causes serious yield losses in wheat (Triticum aestivum) and many other grasses. Race 1 of the fungus, which produces the necrosis toxin Ptr ToxA and the chlorosis toxin Ptr ToxC, is the most prevalent race in the Great Plains of the United States. Wheat genotypes with useful levels of resistance to race 1 have been deployed, but this resistance reduces damage by only 50 to 75%. Therefore, new sources of resistance to P. tritici-repentis are needed. Recombinant inbred lines developed from a cross between the Indian spring wheat cvs. WH542 (resistant) and HD29 (moderately susceptible) were evaluated for reaction to race 1 of the fungus. Composite interval mapping revealed quantitative trait loci (QTL) on the short arm of chromosome 3A explaining 23% of the phenotypic variation, and the long arm of chromosome 5B explaining 27% of the variation. Both resistance alleles were contributed by the WH542 parent. The QTL on 5BL is probably tsn1, which was described previously. The 3AS QTL (QTs.ksu-3AS) on 3AS is a novel QTL for resistance to P. tritici-repentis race 1. The QTL region is located in the most distal bin of chromosome 3AS in a 2.2-centimorgan marker interval. Flanking markers Xbarc45 and Xbarc86 are suitable for marker-assisted selection for tan spot resistance.

scholarly journals Genetic Control of Resistance to Tan Necrosis Induced by Pyrenophora tritici-repentis, Races 1 and 2, in Spring and Winter Wheat Genotypes

2005 ◽  
Vol 95 (2) ◽  
pp. 172-177 ◽  
Author(s):  
P. K. Singh ◽  
G. R. Hughes
Keyword(s):  
Winter Wheat ◽  
Genetic Control ◽  
Recessive Gene ◽  
Tan Spot ◽  
Wheat Genotypes ◽  
Resistant Cultivars ◽  
Pyrenophora Tritici Repentis ◽  
Lesion Type ◽  
Race 1 ◽  
Race 2

The symptoms of tan spot of wheat, caused by Pyrenophora triticirepentis, include a tan necrosis component and an extensive chlorosis component. Since tan spot has become the major component of the leafspotting disease complex of wheat in western Canada, the need for resistant cultivars has increased. This study was conducted to determine whether the resistance to tan spot found in a diverse set of spring and winter wheat genotypes was due to resistance genes not previously reported. The genetic control of resistance to necrosis induced by P. triticirepentis race 1 and race 2 was determined, under controlled environmental conditions, for spring wheat genotypes Erik and 86ISMN 2137 and winter wheat genotypes Hadden, Red Chief, and 6B-365. Plants were inoculated at the two-leaf stage and disease reaction was assessed based on lesion type. Tests of the F1 and F2 generations, and of F2:3 and F2:8 families, indicated that one recessive gene controlled resistance to the necrosis component of tan spot caused by both race 1 and race 2 in each cross studied. Lack of segregation in crosses between the resistant cultivars indicated that the resistance gene was the same in all of the cultivars.

Wheat necrosis induced by Pyrenophora tritici-repentis toxin

1995 ◽  
Vol 53 ◽  
pp. 990-991
Author(s):  
Thomas Freeman ◽  
Jack Rasmussen ◽  
Leonard Francl ◽  
Steve Meinhardt
Keyword(s):  
Molecular Weight ◽  
Crude Extract ◽  
Fungal Pathogen ◽  
Sodium Acetate ◽  
Tan Spot ◽  
Sodium Acetate Buffer ◽  
Dialysis Tubing ◽  
Membrane Breakdown ◽  
Pyrenophora Tritici Repentis ◽  
Fast Flow

Tan spot is a serious foliar disease of wheat caused by Pyrenophora tritici-repentis. This fungal pathogen produces a proteinaceous phytotoxin that induces necrosis in susceptible but not resistant cultivars. Larez et al. reported generalized membrane breakdown and cell death in advance of fungal spread, an effect presumably due to excreted fungal products, including the necrosis toxin. The direct ultrastructural effects of necrosis toxin isolated from P. tritici-repentis have not been previously examined.Crude extract from a culture of isolate 86-124 (1) was thawed and centrifuged for 20 min at 35O00g. The supernatant was filtered through a 0.45 μm Whatman nylon filter and placed in dialysis tubing with a 3,500 molecular weight cut off. The crude extract was dialyzed overnight against 10 volumes of 20 mM sodium acetate buffer, pH 4.8. The dialyzed extract was loaded onto a fresh 10 ml S-sepharose Fast Flow column (Pharmacia) previously equilibrated with 20 mM sodium acetate.

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