A DNA marker for the Bt-10 common bunt resistance gene in wheat

Genome ◽  
1996 ◽  
Vol 39 (1) ◽  
pp. 51-55 ◽  
Author(s):  
T. Demeke ◽  
A. Laroche ◽  
D. A. Gaudet

The Bt-10 bunt gene confers resistance to most races of the common bunt fungi, Tilletia tritici and T. laevis. The RAPD technique, employing a total of 965 decamer primers, was used to identify polymorphic markers between resistant (BW553) and susceptible ('Neepawa') near-isogenic lines. Primer 196 (5′ CTC CTC CCC C 3′) produced a 590 base pair (bp) reproducible fragment only in the resistant near-isogenic line. The 590-bp DNA fragment was present in all the 22 wheat cultivars known to carry the Bt-10 resistance gene and also in 15 resistant F2 lines obtained from a cross between the resistant parent, BW553, and the susceptible parent, 'Neepawa'. The 590-bp fragment was absent in 16 susceptible cultivars tested and in 15 susceptible F2 lines obtained from the cross described above. These results suggest a close linkage between the presence of the 590-bp fragment and the Bt-10 resistance gene. Primer 372 (5′ CCC ACT GAC G 3′) amplified a 1.0-kilobase (kb) fragment that was present only in the susceptible near-isogenic line. This 1.0-kb fragment was present in 13 of the 16 susceptible cultivars and in 13 of the 15 susceptible F2 lines. However, the primer also amplified the 1.0-kb fragment in some resistant cultivars and resistant F2 lines, suggesting a looser linkage between the occurrence of the fragment and the susceptible allele. Key words : RAPD, primer, Bt-10 bunt resistance gene, wheat, marker.

Genome ◽  
2000 ◽  
Vol 43 (2) ◽  
pp. 217-223 ◽  
Author(s):  
André Laroche ◽  
Tigst Demeke ◽  
Denis A Gaudet ◽  
Byron Puchalski ◽  
Michelle Frick ◽  
...  

In western Canada, the Bt-10 resistance gene in wheat (Triticum aestivum) is effective against all the known races of common bunt caused by Tilletia tritici and T. laevis. The genotypes of 199 F2 plants, originated from a cross between BW553 containing Bt-10 and the susceptible spring wheat cultivar 'Neepawa,' were established in greenhouse and field inoculation studies. A ratio of 1:2:1 resistant : heterozygous : susceptible was observed for bunt reaction, indicating that Bt-10 was expressed in a partially dominant fashion. A polymorphic DNA fragment, amplified using RAPD, and previously shown to be linked to Bt-10 was sequenced and SCAR (sequence characterized amplified region) primers devised. However, SCAR primers failed to amplify the polymorphic fragment. Restriction of PCR products with DraI revealed a polymorphic fragment of 490 bp resulting from a single base pair difference between lines possessing Bt-10 and those lacking the gene. As per the base pair difference, FSD and RSA primers were designed to generate a 275-bp polymorphic DNA fragment. Both 275- and 490-bp polymorphic fragments were present in all of the 22 cultivars known to carry Bt-10, and absent in all 16 cultivars lacking Bt-10. A 3:1 ratio was observed for presence: absence of the 275-bp marker in the F2 population. Using Southern analysis, the 490-bp fragment was effective in differentiating homozygous resistant plants from those heterozygous for Bt-10, based on its presence and the hybridization signal strength. A 1:2:1 resistant : heterozygous : susceptible ratio was also observed for the molecular marker and corresponded to 88% of the phenotypes deduced from the original F2 population. The molecular marker was estimated to be between 1.1 cM and 6.5 cM away from the Bt-10 resistance gene, based on the segregation analysis. Segregation analyses of Bt-10 and the 275-bp marker, evaluated in three different Canada Prairie Spring (CPS) wheat populations, demonstrated a segregation ratio of 3:1 for the molecular marker in two of the populations. These results demonstrated that the PCR marker system using the FSD and RSA primer pair permitted a rapid and reliable identification of individual lines carrying the Bt-10 gene for resistance to common bunt. Key words: resistance gene, genetic segregation, molecular marker, RAPD analysis.


2006 ◽  
Vol 86 (Special Issue) ◽  
pp. 1409-1412 ◽  
Author(s):  
J. G. Menzies ◽  
R. E. Knox ◽  
Z. Popovic ◽  
J. D. Procunier

Knowledge of the chromosomal location of disease resistance genes assists in their identification and classification. The determination of the chromosomal location in wheat of the common bunt (Tilletia tritici and T. laevis) resistance gene Bt10 was the goal of this study. Doubled haploid lines were developed from a cross between bunt susceptible Glenlea and bunt resistant AC Taber carrying Bt10. The doubled haploid lines were inoculated with T. tritici race T19, grown in a growth room and rated for bunt near maturity. A series of 50 wheat microsatellite markers were tested on DNA of the individual lines. The population segregated 1:1 for bunt reaction with clear separation between resistant and susceptible classes. A trait related DNA polymorphism generated by gwm469 located in chromosome 6D fit a 1:1 segregation. Combined segregation of bunt resistance and the gwm469 polymorphism differed significantly from a 1:1: 1:1 ratio with a preponderance of parental types confirming linkage of gwm469 with Bt10. The map distance between gwm469 and Bt10was estimated at 19.3 cM by MAPMAKER. The microsatellite markers wmc749, barc54 and cfd0033, located on chromosome 6D, also were significantly associated with the bunt resistance and gwm469. In total, six markers previously located to chromosome 6D were in the linkage group with the Bt10 common bunt resistance. The linkage of these markers with each other and Bt10 indicated that Bt10 is located on the short arm of chromosome 6D. Key words: Tilletia tritici, Tilletia laevis, Triticum aestivum, wheat, microsatellite, doubled haploid


Euphytica ◽  
2020 ◽  
Vol 216 (5) ◽  
Author(s):  
Almuth Elise Muellner ◽  
Babur Eshonkulov ◽  
Julia Hagenguth ◽  
Bernadette Pachler ◽  
Sebastian Michel ◽  
...  

2017 ◽  
Vol 130 (5) ◽  
pp. 1031-1040 ◽  
Author(s):  
Philipp Matthias Steffan ◽  
Anna Maria Torp ◽  
Anders Borgen ◽  
Gunter Backes ◽  
Søren K. Rasmussen

2009 ◽  
Vol 119 (3) ◽  
pp. 541-553 ◽  
Author(s):  
Shu Wang ◽  
Ronald E. Knox ◽  
Ronald M. DePauw ◽  
Fran R. Clarke ◽  
John M. Clarke ◽  
...  

2009 ◽  
Vol 22 (11) ◽  
pp. 1366-1378 ◽  
Author(s):  
Haiyan Jia ◽  
Seungho Cho ◽  
Gary J. Muehlbauer

Fusarium head blight (FHB), caused primarily by Fusarium graminearum, decreases grain yield and quality in wheat and barley. Disease severity, deoxynivalenol (DON), fungal biomass, and transcript accumulation were examined in a wheat near-isogenic line pair carrying either the resistant or susceptible allele for the chromosome 3BS FHB-resistance quantitative trait locus (Fhb1). Fhb1 restricts spread of disease symptoms but does not provide resistance to initial infection or initial DON accumulation. Wheat exhibits both induction and repression of large sets of gene transcripts during F. graminearum infection. In addition, a difference in the general timing of transcript accumulation in plants carrying either the resistant or susceptible allele at the Fhb1 locus was detected, and 14 wheat gene transcripts were detected that exhibited accumulation differences between the resistant and susceptible alleles. These results indicate that these may be host responses that differentiate the resistant from the susceptible interaction. Comparative analysis of the wheat–F. graminearum and the barley–F. graminearum interactions revealed a large set of conserved transcript accumulation patterns. However, we also detected gene transcripts that were repressed in wheat but not in barley. Based on the disease symptoms, transcript accumulation data, and comparative analysis of the barley and wheat host response to F. graminearum infection, we developed an integrated model for the interactions of wheat and barley with F. graminearum.


2019 ◽  
Vol 132 (11) ◽  
pp. 3023-3033 ◽  
Author(s):  
Firdissa E. Bokore ◽  
Richard D. Cuthbert ◽  
Ron E. Knox ◽  
Arti Singh ◽  
Heather L. Campbell ◽  
...  

2007 ◽  
Vol 97 (11) ◽  
pp. 1397-1405 ◽  
Author(s):  
Denis A. Gaudet ◽  
Zhen-Xiang Lu ◽  
Frances Leggett ◽  
Bryan Puchalski ◽  
André Laroche

The infection of wheat lines Neepawa (susceptible), and its sib BW553 that is nearly isogenic for the Bt-10 resistance gene by differentially virulent races T1 and T27 of common bunt (Tilletia tritici), was followed for 21 days following seeding (dfs) using fluorescence and confocal microscopy. Spore germination was nonsynchronous and all spore stages including germination were observed 5 to 21 dfs. Initial host perception of pathogen invasion, based on autofluorescence in epidermal cells adjacent to the appressoria, was similar in both compatible and incompatible interactions, and occurred as early as 5 to 6 dfs. The total number of sites on a 1-cm segment of coleoptile adjacent to the seed that exhibited autofluorescence was similar in both the compatible and incompatible interactions and rose to a maximum of 35 to 40 per 1 cm length of coleoptile following 17 dfs, although new infection events were observed as late as 21 dfs. In the compatible interaction, the autofluorescence became more diffuse 10 to 12 dfs, emanating in all directions in association with fungal spread. In the incompatible interaction, autofluorescence remained restricted to a small area surrounding the penetration site. Two different reaction zones that extended further in tissues surrounding the penetration point in the incompatible interaction compared with the compatible interaction were identified. The accumulation of callose around invading fungal hyphae was observed during both the compatible and incompatible interactions from 8 to 21 dfs. While callose accumulation was more extensive and widespread in the incompatible interaction, it was clearly present in compatible interactions, particularly in treatments involving BW553. These results were confirmed by expression of callose synthase transcripts that were more abundant in BW553 than in Neepawa and were upregulated during pathogen infection in both compatible and incompatible interactions.


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