scholarly journals Reaction of Ptr ToxA-Insensitive Wheat Mutants to Pyrenophora tritici-repentis Race 1

2002 ◽  
Vol 92 (1) ◽  
pp. 38-42 ◽  
Author(s):  
T. L. Friesen ◽  
J. B. Rasmussen ◽  
C. Y. Kwon ◽  
L. J. Francl ◽  
S. W. Meinhardt

The host-selective toxin Ptr ToxA is produced by races 1 and 2 of Pyrenophora tritici-repentis, causal agent of tan spot of wheat. Ptr ToxA has been causally associated with pathogenicity by the race 2 phenotype in this system. However, the role of toxin in disease caused by race 1, the most prevalent form of the fungus in the central and northern Great Plains of North America, has not been rigorously investigated. Three independent wheat lines harboring mutations for insensitivity to Ptr ToxA were derived from ethylmethane sulfonate treatment of the hard red spring wheat cv. Kulm, possessing the single dominant gene for toxin sensitivity. Each of the three mutants was insensitive to Ptr ToxA in bioassays based on necrosis development and electrolyte leakage. Each mutant was crossed to each of the other mutants and to the wild-type Kulm. Segregation data indicate that each mutant line harbors a single recessive mutation for toxin insensitivity that maps to or near the same locus, possibly the toxin-sensitivity gene. Each toxin-insensitive mutant line was susceptible to two isolates of race 1 of P. tritici-repentis. F2 and F3 generations derived from crosses between Kulm and each mutant segregated for toxin reaction. However, segregation for fungal reaction was not evident, and all F3 families were tan spot susceptible regardless of toxin reaction. Host insensitivity to Ptr ToxA is not necessarily equivalent to resistance to race 1. Ptr ToxA should not be used alone as a proxy for fungal inoculations by breeding programs aimed at developing tan spot-resistant wheat.

Plant Disease ◽  
2008 ◽  
Vol 92 (1) ◽  
pp. 91-95 ◽  
Author(s):  
Sukhwinder Singh ◽  
William W. Bockus ◽  
Indu Sharma ◽  
Robert L. Bowden

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.


2001 ◽  
Vol 81 (3) ◽  
pp. 519-525 ◽  
Author(s):  
S. D. Duguid ◽  
A. L. Brûlé-Babel

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


Plant Disease ◽  
2015 ◽  
Vol 99 (10) ◽  
pp. 1333-1341 ◽  
Author(s):  
Zhaohui Liu ◽  
Ibrahim El-Basyoni ◽  
Gayan Kariyawasam ◽  
Guorong Zhang ◽  
Allan Fritz ◽  
...  

Tan spot and Stagonospora nodorum blotch (SNB), often occurring together, are two economically significant diseases of wheat in the Northern Great Plains of the United States. They are caused by the fungi Pyrenophora tritici-repentis and Parastagonospora nodorum, respectively, both of which produce multiple necrotrophic effectors (NE) to cause disease. In this work, 120 hard red winter wheat (HRWW) cultivars or elite lines, mostly from the United States, were evaluated in the greenhouse for their reactions to the two diseases as well as NE produced by the two pathogens. One P. nodorum isolate (Sn4) and four Pyrenophora tritici-repentis isolates (Pti2, 331-9, DW5, and AR CrossB10) were used separately in the disease evaluations. NE sensitivity evaluation included ToxA, Ptr ToxB, SnTox1, and SnTox3. The numbers of lines that were rated highly resistant to individual isolates ranged from 11 (9%) to 30 (25%) but only six lines (5%) were highly resistant to all isolates, indicating limited sources of resistance to both diseases in the U.S. adapted HRWW germplasm. Sensitivity to ToxA was identified in 83 (69%) of the lines and significantly correlated with disease caused by Sn4 and Pti2, whereas sensitivity to other NE was present at much lower frequency and had no significant association with disease. As expected, association mapping located ToxA and SnTox3 sensitivity to chromosome arm 5BL and 5BS, respectively. A total of 24 potential quantitative trait loci was identified with −log (P value) > 3.0 on 12 chromosomes, some of which are novel. This work provides valuable information and tools for HRWW production and breeding in the Northern Great Plains.


2003 ◽  
Vol 93 (4) ◽  
pp. 397-401 ◽  
Author(s):  
T. L. Friesen ◽  
S. Ali ◽  
S. Kianian ◽  
L. J. Francl ◽  
J. B. Rasmussen

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.


2019 ◽  
Vol 22 (8) ◽  
pp. 978-986 ◽  
Author(s):  
A. М. Kokhmetova ◽  
Sh. Ali ◽  
Z. Sapakhova ◽  
M. N. Atishova

Pyrenophora tritici-repentis(Ptr) is the causative agent of tan spot, one of the yield limiting diseases of wheat, rapidly increasing in wheat growing countries including Kazakhstan. The aim of this study was the identifcation of wheat genotypes with resistance to Ptr race 1 and race 5 and their host­selective effectors (toxins) Ptr ToxA and Ptr ToxB. A common wheat collection of 41 accessions (38 experimental and 3 controls) was characterized using the molecular markersXfcp623andXBE444541, diagnostic for theTsn1andTsc2genes conferring sensitivity to fungal toxins. The coincidence of the markerXBE444541with resistance to race 5 was 92.11 %, and with Ptr ToxB, 97.37 %. Genotyping results using the markerXfcp623confrmed the expected response to Ptr ToxA; the presence/absence of the markerXfcp623completely (100 %) coincided with sensitivity/resistance to race 1 and Ptr ToxA. This demonstrates the reliability of the diagnostic markerXfcp623for identifying wheat genotypes with resistance to the fungus and insensitivity to Ptr ToxA. The study of the reaction of wheat germplasm to the fungal inoculation and toxin infltration showed that out of 38 genotypes analyzed 30 (78 %) exhibited resistance to both race 1 and race 5, and insensitivity to toxins Ptr ToxA and ToxB. Of most signifcant interest are eight wheat genotypes that showed resistance/insensitivity both to the two races and two toxins. The results of phenotyping were reconfrmed by the molecular markers used in this study. Sensitivity to Ptr ToxB is not always correlated with susceptibility to race 5 and is dependent on the host’s genetic background of the wheat genotype, i. e. on a specifc wheat genotype. The results of the study are of interest for increasing the efciency of breeding based on the elimination of the genotypes with the dominant allelesTsn1andTsc2sensitive to the toxins Ptr ToxA and ToxB. The genotypes identifed will be used in wheat breeding for resistance to tan spot.


2020 ◽  
Vol 24 (7) ◽  
pp. 722-729
Author(s):  
A. M. Kokhmetova ◽  
N. M. Kovalenko ◽  
M. T. Kumarbaeva

Pyrenophora tritici-repentis is a causative agent of tan spot in wheat. In recent years, there has been an increasing spread and harmfulness of wheat tan spot. The aim of the research was to study the racial composition of the P. tritici-repentis population in the Republic of Kazakhstan. A collection of 30 common wheat accessions, including promising lines and cultivars from Kazakhstan and CIMMYT–ICARDA, was assessed for resistance to P. triticirepentis in a greenhouse and characterized using the Xfcp623 molecular marker, diagnostic for the Tsn1 gene. Monosporic isolates of P. tritici-repentis isolated from the southeastern region were assigned to certain races based on the manifestation of symptoms of necrosis/chlorosis on standard differentials (Glenlea, 6B662, 6B365). Five races of P. tritici-repentis have been identified, including races 1, 2, 3, 7 and 8. It has been shown that races 1 and 8 of P. tritici-repentis are dominant. As a result of the analysis of the frequency of occurrence of the P. tritici-repentis races, it was found that race 1 (50 %) producing Ptr ToxA and Ptr ToxB and race 8 (35 %) producing Ptr ToxA, Ptr ToxB and Ptr ToxC turned out to be dominant. From a practical point of view, of greatest interest are 16 wheat samples, which demonstrated resistance to race 1 and confirmed insensitivity to Ptr ToxA in a molecular screening. These include eight Kazakhstani (4_PSI, 10204_2_KSI, 10204_3_KSI, 10205_2_KSI, 10205_3_KSI, 605_SP2, 632_SP2, Dana) and seven foreign lines (KR11-20, KR11-03, KR11-9014, 11KR-13, KR12-9025, KR12-07, GN-68/2003). The results of this study are of interest in wheat breeding programs for tan spot resistance.


2010 ◽  
Vol 100 (5) ◽  
pp. 468-473 ◽  
Author(s):  
Xiao-Chun Sun ◽  
William Bockus ◽  
Guihua Bai

Tan spot, caused by Pyrenophora tritici-repentis, is an economically important foliar disease of wheat worldwide. Eight races of the pathogen have been characterized on the basis of their ability to cause necrosis or chlorosis in a set of differential wheat lines. Race 1 produces two host-selective toxins, Ptr ToxA and Ptr ToxC, that induce necrosis and chlorosis, respectively, on leaves of sensitive wheat genotypes. A population of recombinant inbred lines was developed from a cross between Chinese landrace Wangshuibai (resistant) and Chinese breeding line Ning7840 (highly susceptible) to identify chromosome regions harboring quantitative trait loci (QTL) or genes for tan spot resistance. Plants were inoculated at the four-leaf stage in a greenhouse and percent leaf area diseased was scored 7 days after inoculation. Two QTL for resistance to race 1 were mapped to the short arms of chromosomes 1A and 2B in the population. The QTL on 1AS, designated as QTs.ksu-1AS, showed a major effect and accounted for 39% of the phenotypic variation; the QTL on 2BS, designated as QTs.ksu-2BS, explained 4% of the phenotypic variation for resistance. A toxin infiltration experiment demonstrated that both parents were insensitive to Ptr ToxA, suggesting that the population was most likely segregating for reaction to chlorosis, not necrosis. The markers closely linked to the QTL should be useful for marker-assisted selection in wheat-breeding programs.


2008 ◽  
Vol 98 (6) ◽  
pp. 702-708 ◽  
Author(s):  
P. K. Singh ◽  
M. Mergoum ◽  
S. Ali ◽  
T. B. Adhikari ◽  
G. R. Hughes

Tan spot of wheat, caused by the fungus Pyrenophora tritici-repentis, is a destructive disease worldwide that can lead to serious losses in quality and quantity of wheat grain production. Resistance to multiple races of P. tritici-repentis was identified in a wide range of genetically diverse genotypes, including three different species Triticum aestivum (AABBDD), T. spelta (AABBDD), and T. turgidum (AABB). The major objectives of this study were to determine the genetic control of resistance to P. tritici-repentis races 1 and 5 in 12 newly identified sources of resistance. The parents, F1, F2, and F2:3 or F2:5 families of each cross were analyzed for the allelism tests and/or inheritance studies. Plants were inoculated at the two-leaf stage under controlled environmental conditions and disease reaction was assessed based on lesion-type rating scale. A single recessive gene controlled resistance to necrosis caused by P. tritici-repentis race 1 in both tetraploid and hexaploid resistant genotypes. The lack of segregation in the inter- and intra-specific crosses between the resistant tetraploid and hexaploid genotypes indicated that they possess the same genes for resistance to tan necrosis and chlorosis induced by P. tritici-repentis race 1. A single dominant gene for chlorosis in hexaploid wheat and a single recessive gene for necrosis in tetraploid wheat, controlled resistance to P. tritici-repentis race 5.


2005 ◽  
Vol 95 (2) ◽  
pp. 172-177 ◽  
Author(s):  
P. K. Singh ◽  
G. R. Hughes

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.


Plant Disease ◽  
2006 ◽  
Vol 90 (10) ◽  
pp. 1320-1325 ◽  
Author(s):  
P. K. Singh ◽  
M. Mergoum ◽  
S. Ali ◽  
T. B. Adhikari ◽  
E. M. Elias ◽  
...  

Tan spot, caused by Pyrenophora tritici-repentis, is a serious foliar disease of wheat (Triticum aestivum) in North America. Control of tan spot through management practices and fungicide application is possible; however, the use of resistant varieties is the most effective and economical means of controlling tan spot. This study was conducted to determine the disease reaction of 126 elite hard red spring, white, and durum wheat varieties and advanced breeding lines collected from the northern Great Plains of the United States and Canada to individual races/toxins of P. tritici-repentis. Seedling evaluation of the 126 genotypes was done under controlled environmental conditions with virulent races 2, 3, and 5 of P. tritici-repentis and toxins Ptr ToxA and Ptr ToxB. Based on disease reactions, two resistant varieties and two advanced breeding lines adapted to the northern Great Plains were found to be resistant to all the races and insensitive to the toxins tested. Additionally, six genetically diverse lines/varieties were identified to be resistant to tan spot; however, these sources may not be well adapted to the northern Great Plains. These results suggest that the wheat germ plasm contains a broad genetic base for resistance to the most prevalent races of P. tritici-repentis in North America, and the resistant sources identified in this study may be utilized in wheat breeding programs to develop tan spot resistant varieties.


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