scholarly journals Identifcation of genotypescarriers of resistance to tan spot Ptr ToxA and Ptr ToxB of Pyrenophora tritici-repentis in common wheat collection

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.


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.


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.


2019 ◽  
Vol 23 (7) ◽  
pp. 879-886 ◽  
Author(s):  
A. M. Kokhmetova ◽  
M. N. Atishova ◽  
M. T. Kumarbayeva ◽  
I. N. Leonova

Tan spot caused by the fungus Pyrenophora tritici-repentis is an important leaf spot disease in wheat growing areas throughout the world. The study aims to identify wheat germplasm resistant to tan spot based on phytopathological screening and molecular marker analysis. A collection of 64 common wheat germplasms, including cultivars and breeding lines from Kazakhstan and CIMMYT, was assessed for tan spot resistance in greenhouse conditions and characterized using the Xfcp623 molecular marker, diagnostic for the Tsn1 gene. All wheat cultivars/lines varied in their reaction to tan spot isolate race 1, ranging from susceptible to resistant. Most accessions studied (53 %) were susceptible to Ptr race 1. Spring wheat cultivars were more susceptible to race 1 than winter wheat cultivars. As a result of genotyping, an insensitive reaction to Ptr ToxA was predicted in 41 wheat cultivars (64 %). The tsn1 gene carriers identified included 27 Kazakhstani and 14 CIMMYT cultivars/lines, demonstrating insensitivity to Ptr ToxA. The majority of the Tsn1 genotype were sensitive to race 1 and showed susceptibility to the pathogen in the field. Disease scores from seedling stage positively correlated with field disease ratings. Of particular interest are 27 wheat accessions that demonstrated resistance to spore inoculation by Ptr race 1, were characterized by insensitivity to ToxA and showed field resistance to the pathogen. The results of this study will contribute to wheat breeding programs for tan spot resistance with Marker Assisted Selection using the closely flanking markers.


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.


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


2005 ◽  
Vol 95 (2) ◽  
pp. 144-152 ◽  
Author(s):  
Lakhdar Lamari ◽  
Brent D. McCallum ◽  
Ron M. dePauw

Pyrenophora tritici-repentis causes necrosis and chlorosis in its wheat host. Susceptibility to races 2 (necrosis) and 5 (chlorosis) of the pathogen is known to be mediated by Ptr ToxA and Ptr ToxB, respectively. Sensitivity to each toxin is controlled by a single dominant and independently inherited gene. We used sensitivity to Ptr ToxA and Ptr ToxB as two genetic markers to investigate the origin and the state of tan spot susceptibility in Canadian Western Red Spring (CWRS) wheat over a period of more than a century. Sensitivity to Ptr ToxA, the toxin produced by nearly all isolates of the pathogen collected in the past 20 years in western Canada, appears to have been present in the first major cultivar, Red Fife, grown massively in the late 1800s. Sensitivity then was transmitted unknowingly into Canadian wheat lines through extensive use of backcrossing to maintain the Marquis-Thatcher breadmaking quality. Sensitivity to Ptr ToxA, which nearly disappeared from cultivars grown in western Canada in the 1950s, was reintroduced in the 1960s and unintentionally bred into many of the present-day cultivars. Sensitivity to Ptr ToxB, a toxin rarely found in isolates from western Canada, appeared with the release of Thatcher in 1934 and was transferred to many cultivars through backcross programs. In spite of large areas planted to Ptr ToxAand Ptr ToxB-sensitive cultivars over decades, tan spot epidemics remained sporadic until the 1970s. The results of this study raise the problem of the narrowing genetic base of CWRS wheat lines and the potential for unanticipated threats from plant pathogens. The intercrossing of genetically diverse material in one Canadian wheat breeding program resulted in the release of several modern cultivars with resistance to tan spot. The absence of wild-type Ptr ToxB-producing isolates in western Canada remains unexplained, given that sensitivity to Ptr ToxB was present continuously in western Canadian cultivars grown on vast areas for more than 70 years.


2020 ◽  
Vol 384 (2) ◽  
pp. 29-35
Author(s):  
A. Kokhmetova ◽  
M. Atishova

Intensified wheat production, changes in cultural practices including shifts from conventional tillage to reduced tillage practices, and wheat monoculture involving cultivation of susceptible cultivars has resulted in development of tan spot to epidemic proportions in Kazakhstan. Pyrenophora tritici-repentis, causal agent of tan spot on wheat. In recent years, there has been increasing distribution and harmfulness of P. tritici-repentis on wheat. The aim of the study was to identify and select wheat germplasm resistant to tan spot P. tritici-repentis using molecular markers. The results of field evaluation showed resistant reaction to tan spot in 76 wheat varieties (68%). Molecular screening of wheat germplasm was carried out based on the reaction to the fungal inoculum and to host-specific toxins (HST) produced by the P. tritici-repentis. The wheat germplasm insensitive to the toxins HST Ptr ToxA and Ptr ToxB was selected. As a result of molecular screening of 111 wheat genotypes using SSR marker Xfcp623 linked to insensitivity gene to the selective toxin Ptr ToxA of tan spot, 31 carriers of effective tsn1 gene were identified, which accounted for 27,9% of the genotypes studied. Ten samples of wheat (Jubileynaya 60, TOO11/TOOOO7, F3.71/TRM/VORONA/3/OC14, NANJTNG 82149 KAUZ, ECHA/LI115, Akmola 2, Kazakh-stanskaya rannespelaya, Kazakhstanskaya 25, 428g/MK-122A and 190-Naz/GF55) are characterized with complex resistance to the races Ptr 1 and 5, as well as to 2 toxins (ToxA and ToxB) and to the Septoria nodorum blotch isolate SNB7k. 20 promising wheat lines resistant to tan spot were selected. These genotypes also showed a moderate and high level of field resistance and recommended to use in the breeding programs for resistance to tan spot.


THE BULLETIN ◽  
2020 ◽  
Vol 2 (384) ◽  
pp. 29-35
Author(s):  
A. Kokhmetova ◽  
◽  
M. Atishova ◽  
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