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 CHROMOSOMAL LOCATION OF GENES CONTROLLING FLAVONOID PRODUCTION IN HEXAPLOID WHEAT

Genetics ◽  
1983 ◽  
Vol 103 (2) ◽  
pp. 313-321
Author(s):  
Paula R Neuman ◽  
J G Waines ◽  
K W Hilu ◽  
D Barnhart
Keyword(s):  
Triticum Aestivum ◽  
Hexaploid Wheat ◽  
Chinese Spring ◽  
Chromosomal Location ◽  
Triticum Aestivum L ◽  
Phenolic Glycoside ◽  
Two Dimensional ◽  
Chromosome Arm ◽  
The Individual ◽  
Homoeologous Chromosomes

ABSTRACT Two-dimensional paper chromatography was performed on methanol extracts of leaves of hexaploid bread wheat, Triticum aestivum L. em. Thell. cultivar Chinese Spring, and of the available nullisomic-tetrasomic compensating lines, the tetrasomic lines and the ditelocentric lines. The chromatograms had 27 spots identified as flavonoids and six representing phenolic acids. Some of the areas were complex and contained more than one compound. Four flavonoids were identified as under the control of gene(s) on chromosome arms 1DS, 4DL, 5AS and 6BS. A phenolic glycoside was concluded to be controlled by a gene(s) on chromosome arm 7BL. Gene(s) on chromosome arm 4DL affected the amount of compounds in two other spots, and gene(s) on chromosome arm 4BS reduced the level of all flavonoid compounds. The individual compounds in some of the complex spots may be under the control of gene(s) on homoeologous chromosomes.

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 IDENTIFICATION OF THREE CHROMOSOMAL INTERCHANGES IN COMMON WHEAT, TRITICUM AESTIVUM L.

1974 ◽  
Vol 16 (2) ◽  
pp. 349-354 ◽  
Author(s):  
A. C. Baier ◽  
F. J. Zeller ◽  
G. Fischbeck
Keyword(s):  
Triticum Aestivum ◽  
Powdery Mildew ◽  
Single Cell ◽  
Resistance Gene ◽  
Common Wheat ◽  
Chinese Spring ◽  
Powdery Mildew Resistance ◽  
Triticum Aestivum L ◽  
Powdery Mildew Resistance Gene ◽  
Segregation Ratios

Analyzing the F1 P.M.C.s of the crosses between Solo and the 21 monosomic lines of Chinese Spring three chromosomal interchanges involving six wheat chromosomes were identified. 5B/7B involves the longest segments and is already known in other varieties. 7A/7D involves a powdery mildew resistance gene, probably Pm 1 on the distal end of the long arm of chromosome 7A. An attempt is made to explain the deviating segregation ratios of these two aneuploid F2's in the mildew tests. 2A/4D probably involves very short segments since only one single cell out of 1,400 P.M.C.s showed three quadrivalents.

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

Markers to a common bunt resistance gene derived from ‘Blizzard’ wheat (Triticum aestivum L.) and mapped to chromosome arm 1BS

2009 ◽  
Vol 119 (3) ◽  
pp. 541-553 ◽  
Author(s):  
Shu Wang ◽  
Ronald E. Knox ◽  
Ronald M. DePauw ◽  
Fran R. Clarke ◽  
John M. Clarke ◽  
...  
Keyword(s):  
Triticum Aestivum ◽  
Resistance Gene ◽  
Triticum Aestivum L ◽  
Common Bunt ◽  
Chromosome Arm ◽  
Bunt Resistance

CHROMOSOME LOCATION OF GENES CONDITIONING RESISTANCE TO CLAVICEPS PURPUREA IN SPRING AND DURUM WHEAT

1977 ◽  
Vol 19 (4) ◽  
pp. 679-682 ◽  
Author(s):  
R. G. Platford ◽  
C. C. Bernier ◽  
L. E. Evans
Keyword(s):  
Triticum Aestivum ◽  
Durum Wheat ◽  
Chinese Spring ◽  
Triticum Aestivum L ◽  
Claviceps Purpurea ◽  
Chromosome Location ◽  
Resistant Reaction ◽  
Or Genes ◽  
Chromosome 3B ◽  
Three Components

The chromosome location of genes conferring resistance to Claviceps purpurea (Fr.) Tul. in Triticum aestivum L. cv. Kenya Farmer and T. durum Desf. cv. Carleton was determined. A substitution series of individual chromosomes of Kenya Farmer into the susceptible T. aestivum cv. Chinese Spring and the F1 plants of Carleton crossed with the Chinese Spring monosomics for the A and B genomes were used. Chromosome 6B of Kenya Farmer and 1B of Carleton appeared to carry a gene or genes conditioning resistance to all three components of the resistant reaction, i.e. frequency and size of sclerotia and honeydew production. In addition, chromosome 3B of Carleton appeared to reduce the sclerotia frequency and honeydew production while several chromosomes of both Kenya Farmer and Carleton influenced sclerotia size and honeydew production.

The chromosome location of four recombinants between Agropyron chromosome 7el2 and a wheat chromosome

Genome ◽  
1988 ◽  
Vol 30 (1) ◽  
pp. 97-98 ◽  
Author(s):  
D. R. Knott
Keyword(s):  
Triticum Aestivum ◽  
Stem Rust ◽  
Rust Resistance ◽  
Wheat Chromosome ◽  
Triticum Aestivum L ◽  
Puccinia Graminis ◽  
Monosomic Analysis ◽  
Chromosome Location ◽  
Homoeologous Recombination ◽  
Puccinia Graminis Tritici

Four stem rust (Puccinia graminis tritici Eriks. &Henn.) resistant wheat (Triticum aestivum L.) – Agropyron recombinants were analyzed to determine the wheat chromosomes involved. The Agropyron chromosome, 7el2, was known to be homoeologous to the group 7 chromosomes of wheat. Monosomic analysis showed that all four recombinants involved wheat chromosome 7D.Key words: rust resistance, Puccinia, Agropyron, wheat, Triticum, homoeologous recombination.

Chilling injury and chlorotic reactions of euploids and aneuploids of the group 6 homoeologues of common wheat

Genome ◽  
1992 ◽  
Vol 35 (3) ◽  
pp. 468-473 ◽  
Author(s):  
Ernest D. P. Whelan ◽  
G. B. Schaalje
Keyword(s):  
Triticum Aestivum ◽  
Common Wheat ◽  
Chinese Spring ◽  
Prolonged Exposure ◽  
Chilling Injury ◽  
Triticum Aestivum L ◽  
Recessive Trait ◽  
Cytoplasmic Effects ◽  
Group 6 ◽  
Winter Wheat Cultivars

Aneuploid seedlings of the common wheat (Triticum aestivum L.) cv. Chinese Spring (CS) that are nullisomic or telosomic for the long arm of chromosome 6D are susceptible to chilling injury under prolonged exposure to 6 °C; normal euploids or telosomics for the short arm are not. Studies of seedling grown for various durations at 20 °C prior to growth at 6 °C showed that chilling injury was a juvenile phenomenon and that the extent of injury was inversely proportional to the duration of growth at 20 °C to a maximum of about 14 days. When reciprocal crosses were made between susceptible 6D nullisomics or long-arm ditelocentrics of CS and resistant 6D nullisomics of three spring and one winter wheat cultivars, progenies from aneuploid F1 hybrids all segregated for susceptibility as a recessive trait and at a frequency approximating a dihybrid ratio; no cytoplasmic effects were detected. Aneuploids of the group 6 homoeologues of the spring wheat cvs. Cadet and Rescue were resistant, as were group 6 whole-chromosome substitutions of eight different donor wheats in the recipient parent CS and 56 other euploids tested. Genes for resistance to chilling injury appear to involve the group 6 chromosomes and the short arm of 6D in Chinese Spring. In contrast with chilling injury, all aneuploid lines with only four doses of the "corroded" loci on group 6 chromosomes exhibited chlorotic symptoms.Key words: Triticum aestivum, chilling injury.

scholarly journals Identification and Molecular Mapping of a Gene Conferring Resistance to Pyrenophora tritici-repentis Race 3 in Tetraploid Wheat

2006 ◽  
Vol 96 (8) ◽  
pp. 885-889 ◽  
Author(s):  
P. K. Singh ◽  
J. L. Gonzalez-Hernandez ◽  
M. Mergoum ◽  
S. Ali ◽  
T. B. Adhikari ◽  
...  
Keyword(s):  
Resistance Genes ◽  
Molecular Mapping ◽  
Recombinant Inbred Lines ◽  
Tetraploid Wheat ◽  
Recessive Gene ◽  
Tan Spot ◽  
Substitution Lines ◽  
Disease Reaction ◽  
Pyrenophora Tritici Repentis ◽  
The Cross

Race 3 of the fungus Pyrenophora tritici-repentis, causal agent of tan spot, induces differential symptoms in tetraploid and hexaploid wheat, causing necrosis and chlorosis, respectively. This study was conducted to examine the genetic control of resistance to necrosis induced by P. tritici-repentis race 3 and to map resistance genes identified in tetraploid wheat (Triticum turgidum). A mapping population of recombinant inbred lines (RILs) was developed from a cross between the resistant genotype T. tur-gidum no. 283 (PI 352519) and the susceptible durum cv. Coulter. Based on the reactions of the Langdon-T. dicoccoides (LDN[DIC]) disomic substitution lines, chromosomal location of the resistance genes was determined and further molecular mapping of the resistance genes for race 3 was conducted in 80 RILs of the cross T. turgidum no. 283/Coulter. Plants were inoculated at the two-leaf stage and disease reaction was assessed 8 days after inoculation based on lesion type. Disease reaction of the LDN(DIC) lines and molecular mapping on the T. turgidum no. 283/Coulter population indicated that the gene, designated tsn2, conditioning resistance to race 3 is located on the long arm of chromosome 3B. Genetic analysis of the F2 generation and of the F4:5 and F6:7 families indicated that a single recessive gene controlled resistance to necrosis induced by race 3 in the cross studied.

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