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 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
Keyword(s):  
Great Plains ◽  
Dominant Gene ◽  
Tan Spot ◽  
Mutant Line ◽  
Northern Great Plains ◽  
Recessive Mutation ◽  
Pyrenophora Tritici Repentis ◽  
Ptr Toxa ◽  
Race 1 ◽  
Toxin Sensitivity

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.

scholarly journals Genetic Analysis of Resistance to Pyrenophora tritici-repentis Races 1 and 5 in Tetraploid and Hexaploid Wheat

2008 ◽  
Vol 98 (6) ◽  
pp. 702-708 ◽  
Author(s):  
P. K. Singh ◽  
M. Mergoum ◽  
S. Ali ◽  
T. B. Adhikari ◽  
G. R. Hughes
Keyword(s):  
Hexaploid Wheat ◽  
Rating Scale ◽  
Dominant Gene ◽  
Tetraploid Wheat ◽  
Recessive Gene ◽  
Tan Spot ◽  
Single Recessive Gene ◽  
Pyrenophora Tritici Repentis ◽  
Wide Range ◽  
Race 1

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.

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.

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.

scholarly journals Inheritance of Resistance to Bacterial Blight in 21 Cultivars of Rice

2003 ◽  
Vol 93 (2) ◽  
pp. 147-152 ◽  
Author(s):  
K. S. Lee ◽  
S. Rasabandith ◽  
E. R. Angeles ◽  
G. S. Khush
Keyword(s):  
Bacterial Blight ◽  
Oryza Sativa L ◽  
Dominant Gene ◽  
Recessive Gene ◽  
Inheritance Of Resistance ◽  
Race 1 ◽  
Group 2 ◽  
Race 2 ◽  
Moderate Resistance ◽  
Group 1

Genetic analysis for resistance to bacterial blight (Xanthomonas oryzae pv. oryzae) of 21 rice (Oryza sativa L.) cultivars was carried out. These cultivars were divided into two groups based on their reactions to Philippine races of bacterial blight. Cultivars of group 1 were resistant to race 1 and those of group 2 were susceptible to race 1 but resistant to race 2. All the cultivars were crossed with TN1, which is susceptible to all the Philippine races of X. oryzae pv. oryzae. F1 and F2 populations of hybrids of group 1 cultivars were evaluated using race 1 and F1 and F2 populations of hybrids of group 2 cultivars were evaluated using race 2. All the cultivars showed monogenic inheritance of resistance. Allelic relationships of the genes were investigated by crossing these cultivars with different testers having single genes for resistance. Three cultivars have Xa4, another three have xa5, one has xa8, two have Xa3, eight have Xa10, and one has Xa4 as well as Xa10. Three cultivars have new, as yet undescribed, genes. Nep Bha Bong To has a new recessive gene for moderate resistance to races 1, 2, and 3 and resistance to race 5. This gene is designated xa26(t). Arai Raj has a dominant gene for resistance to race 2 which segregates independently of Xa10. This gene is designated as Xa27(t). Lota Sail has a recessive gene for resistance to race 2 which segregates independently of Xa10. This gene is designated as xa28(t).

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
Keyword(s):  
Molecular Markers ◽  
Common Wheat ◽  
Wheat Breeding ◽  
Tan Spot ◽  
Wheat Genotype ◽  
Genotype I ◽  
Wheat Genotypes ◽  
Pyrenophora Tritici Repentis ◽  
Ptr Toxa ◽  
Race 1

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.

scholarly journals Genetic Analysis of Meloidogyne arenaria Race 1 Resistance in Tobacco

Plant Disease ◽  
1999 ◽  
Vol 83 (9) ◽  
pp. 810-813 ◽  
Author(s):  
Tenson B. S. Ng'ambi ◽  
Rebeca C. Rufty ◽  
Kenneth R. Barker
Keyword(s):  
Dominant Gene ◽  
Meloidogyne Arenaria ◽  
Block Designs ◽  
Inheritance Of Resistance ◽  
Root Knot Nematode ◽  
Breeding Lines ◽  
Race 1 ◽  
Relationship Of ◽  
Resistant Genotypes ◽  
G 28

Inheritance of resistance to the peanut root-knot nematode (Meloidogyne arenaria (Neal) Chitwood race 1) was investigated in the flue-cured tobacco cv. Speight G 28 and the breeding lines 81-RL-2K and SA 1214. The genetic relationship of this resistance in Speight G 28 to the resistance of the same cultivar to races 1 and 3 of M. incognita was also studied. Crosses were made between the root-knot nematode-susceptible flue-cured tobacco cv. NC 2326 and the three resistant genotypes. Parental, F1, F2 and backcross generations (BC1P1, BC1P2) were grown for each cross in randomized complete block designs with five replications in the greenhouse. Data indicated that resistance to M. arenaria race 1 in the three resistance sources is conditioned by a single dominant gene, but this resistance is partial compared to that for M. incognita races 1 and 3. Further, resistance to races 1 and 3 of M. incognita and resistance to M. arenaria race 1 in cv. Speight G 28 appear to be controlled by the same gene. These results, combined with the absence of segregation in the F2 populations of the crosses between resistant parents 81-RL-2K × SA 1214, 81-RL-2K × Speight G 28, and SA 1214 × Speight G 28, suggest allelism of resistance among these genotypes.

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

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