Development of RAPD markers associated with common bunt resistance to race T1 (Tilletia tritici) in spelt wheat

Common bunt caused by Tilletia tritici and T. laevis has occurred worldwide and reduces yield and quality in common and durum wheats. The development of DNA markers linked to bunt resistance to race T1 in the cross, ‘Laura’(S) בRL5407’ (R), was carried out in this study based on the single head derived F_4:5 and single seed derived F_4:6 populations. Bulked segregant analysis was used to identify two random amplified polymorphic DNA (RAPD) markers linked to the gene for resistance to race T1 in the spelt wheat ‘RL5407′. The two markers identified, UBC548₅₉₀ and UBC274₉₈₈, flanked the resistance gene with a map distance of 9.1 and 18.2 cM, respectively. The former was linked in repulsion phase to bunt resistance while the later was in coupling phase. The two RAPD markers and the common bunt‐resistance gene all segregated in Mendelian fashion. Use of these two RAPD markers together could assist in incorporating the bunt‐resistance gene from spelt wheat into common wheat cultivars by means of marker‐assisted selection.     

Chromosome location of resistance to septoria leaf blotch and common bunt in wheat-barley addition lines

Septoria leaf blotch and common bunt are important diseases of wheat to which Hordeum vulgare is resistant. Addition lines of H. vulgare in wheat were utilized to determine which H. vulgare chromosomes carry resistance genes. Resistance to septoria leaf blotch was conferred by gene(s) present all over the barley genome, but more strongly by those located on chromosomes 7 and 4. Almost complete resistance to common bunt was conferred by gene(s) present in chromosomes 6 and a slight but significant level of resistance was conferred by chromosome 7. This revised version was published online in August 2006 with corrections to the Cover Date.     

A major QTL effect controlling resistance to powdery mildew in winter wheat at the adult plant stage

Powdery mildew is one of the major diseases of wheat in regions with a maritime or semi‐continental climate which can strongly affect grain yield. The objective of the study was to identify and compare quantitative resistance to powdery mildew of line RE9001 at the adult plant and vernalized seedling stages. RE9001 has no known Pm gene and shows a high level of adult plant resistance in the field. Using 104 recombinant inbred lines (RILs) of an RE9001 × ‘Courtot’ F8 population, a genetic map was developed with 363 markers distributed over 26 linkage groups and covering 3825 cM. The global map density was 1 locus/10.3 cM. RILs were assessed under field and tunnel greenhouse conditions for 2 years in two locations. Eleven quantitative trait loci (QTL) were detected at the adult stage and they explained 63% of the variation, depending on the environment. Three QTLs were found, at least, in the two environments. One QTL from RE9001, mapped on chromosome 2B, was stable in each environment. This QTL, QPm.inra.2B, explained 10.3–36.6% of the variation and could be mapped in the vicinity of the Pm6 gene. At the vernalized seedling stage, one QTL detected by the isolate 93‐27 could be an allele of the Pm3g gene present in ‘Courtot’. No residual effect of the Pm3g gene was detected at either stage. Markers flanking the QTL 2B could be useful tools to combine resistance to powdery mildew in wheat cultivars.     

Alleles on the two dwarfing loci on 4B and 4D are main drivers of FHB‐related traits in the Canadian winter wheat population “Vienna” × “25R47”

Fusarium head blight (FHB), leaf rust and stem rust are among the most destructive wheat diseases. High‐yielding, native disease resistance sources are available in North America. The objective of this study was to map loci associated with FHB traits, leaf rust, stem rust and plant height in a “Vienna”/”25R47” population. DArT markers were used to generate a genetic map, and quantitative trait loci (QTL) analysis was performed by evaluating 113 doubled haploid lines across three environments in Ontario, Canada. FHB resistance QTL were identified on chromosomes 4D, 4B, 2D and 7A, while a QTL for leaf and stem rust resistance was identified on chromosome 1B. The dwarfing alleles of both Rht‐B1 and Rht‐D1 were associated with increased FHB index and DON content.     

Molecular mapping re-locates the Stb2 gene for resistance to Septoria tritici blotch derived from cultivar Veranopolis on wheat chromosome 1BS

Septoria tritici blotch (STB) is one of the most destructive foliar diseases in many of the wheat (Triticum aestivum) growing regions of the world. Gene Stb2, derived from cultivar ‘Veranopolis’, provides effective resistance against STB. In our attempts to refine the map location of this resistance gene we could not confirm a previous report that Stb2 is on wheat chromosome 3BS. Instead, based on characterization of the same doubled-haploid population used for the original mapping derived from a cross between Veranopolis and susceptible line RAC875-2, and linkage analysis of the resistance phenotype to previously mapped SSR loci, we report that Stb2 is located on the short arm of wheat chromosome 1B, flanked by microsatellite loci Xwmc406 and Xbarc008 (with Xwmc230 closely located) at map distances of 6 and 5 cM, respectively. Presence of the markers on chromosome arm 1BS was confirmed by analysis of nullisomic-tetrasomic lines. These three co-dominant markers can be used in wheat breeding programs to facilitate combining Stb2 with genes of interest. Other STB resistance genes, including Stb11, have been reported on wheat chromosome arm 1BS, with locus Xbarc008 as a diagnostic marker. Whether Stb2, Stb11 and the previously identified Stb11-like genes are the same, allelic, or different but closely linked has not been determined. In addition to STB, numerous genes for resistance to many other fungal pathogens have been reported on wheat chromosome arm 1BS, including those for yellow (or stripe) rust, leaf rust and common bunt. The approximate locations for all of these genes were added onto the Stb2 map based on published distances from common markers to provide a rough guide for future wheat improvement.     

Mapping of the Vrn-B1 gene in Triticum aestivum using microsatellite markers

An F₂ population segregating for the dominant gene Vrn‐B1 was developed from the cross of the substitution line ‘Diamant/'Miro‐novskaya 808 5A’ and the winter wheat cultivar ‘Bezostaya 1′. Microsatellite markers (Xgwm and Xbarc) with known map locations on chromosome 5B of common wheat were used for mapping the gene Vrn‐B1. Polymorphism between parental varieties was observed for 28 out of 34 microsatellite markers (82%). Applying the quantitative trait loci mapping approach, the target gene was mapped on the long arm of chromosome 5B, closely linked to Xgwm408. The map position of Vrn‐B1 suggests that the gene is homoeologous to other vernalization response genes located on the homoeologous group 5 chromosomes of wheat, rye and barley.     

QTL mapping of a partial resistance to the corn delphacid‐transmitted viruses in Lepidopteran‐resistant maize line Mp705

A partial resistance to maize mosaic virus (MMV) and maize stripe virus (MStV) was mapped in a RILs population derived from a cross between lines MP705 (resistant) and B73 (susceptible). A genetic map constructed from 131 SSR markers spanned 1399 cM with an average distance of 9.6 cM. A total of 10 QTL were detected for resistance to MMV and MStV, using composite interval mapping. A major QTL explaining 34–41% of the phenotypic variance for early resistance to MMV was detected on chromosome 1. Another major QTL explaining up to 30% of the phenotypic variation for all traits of resistance to MStV was detected in the centromeric region of chromosome 3 (3.05 bin). After adding supplementary SSR markers, this region was found to correspond well to the one where a QTL of resistance to MStV already was located in a previous mapping study using an F₂ population derived from a cross between Rev81 and B73. These results suggested that these QTL of resistance to MStV detected on chromosome 3 could be allelic in maize genome.     

Mapping of a gene (Vir) for a non-glaucous, viridescent phenotype in bread wheat derived from Triticum dicoccoides, and its association with yield variation

The introgression of desirable genes or alleles from the wild relatives of hexaploid wheat can be a valuable source of genetic variation for wheat breeders to enhance modern varieties. The UK Group 1 bread making variety Shamrock is an example where the introgression of genetic material from wild emmer (Triticum dicoccoides) has been used to develop a modern cultivar. A striking character of Shamrock is its unique viridescent colour compared to other UK wheats, a trait that coincides with a non-glaucous phenotype. A doubled haploid population segregating for the trait (Shamrock × Shango) was examined to map the location of Vir, and analyse any associated pleiotropic effects. The viridescence gene located to the distal end of the short arm of chromosome 2B. QTL analysis of productivity traits shows an association between Vir and a significant delay in senescence, resulting in an extension of the grain filling period. A stable yield QTL, accounting for up to a quarter of the variation in one case, was also identified at or near Vir, indicating significant yield benefits either by linkage or pleiotropy.     

A quantitative trait locus on chromosome 5B controls resistance of <Emphasis Type="Italic">Triticum turgidum</Emphasis> (L.) var. <Emphasis Type="Italic">diccocoides</Emphasis> to Stagonospora nodorum blotch

Stagonospora nodorum blotch (SNB) is an important foliar disease of durum wheat (Triticum turgidum var. durum) worldwide. The combined effects of SNB and tan spot, considered as components of the leaf spotting disease complex, result in significant damage to wheat production in the northern Great Plains of North America. The main objective of this study was the genetic analysis of resistance to SNB caused by Phaeosphaeria nodorum in tetraploid wheat, and its association with tan spot caused by Pyrenophora tritici-repentis race 2. The 133 recombinant inbred chromosome lines (RICL) developed from the cross LDN/LDN(Dic-5B) were evaluated for SNB reaction at the seedling stage under greenhouse conditions. Molecular markers were used to map a quantitative trait locus (QTL) on chromosome 5B, explaining 37.6% of the phenotypic variation in SNB reaction. The location of the QTL was 8.8 cM distal to the tsn1 locus coding for resistance to P. tritici-repentis race 2. The presence of genes for resistance to both SNB and tan spot in close proximity in tetraploid wheat and the identification of molecular markers linked to these genes or QTLs will be useful for incorporating resistance to these diseases in wheat breeding programs.     

Fusarium head blight resistance derived from Lophopyrum elongatum chromosome 7E and its augmentation with Fhb1 in wheat

The objective of this study was to assess the effectiveness of Fusarium head blight (FHB) resistance derived from wheatgrass Lophopyrum elongatum chromosome 7E and to determine whether this resistance can augment resistance in combination with other FHB resistance quantitative trait loci (QTL) or genes in wheat. The ‘Chinese Spring’–Lophopyrum elongatum disomic substitution line 7E(7B) was crossed to three wheat lines: ‘Ning 7840’, L3, and L4. F₂ populations were evaluated for type II resistance with the single‐floret inoculation method in the greenhouse. Simple sequence repeat markers associated with Fhb1 in ‘Ning 7840’ and L4 and markers located on chromosome 7E were genotyped in each population. Marker–trait association was analysed with one‐way or two‐way analysis of variance. The research showed that, in the three populations, the average number of diseased spikelets (NDS) in plants with chromosome 7E is 1.2, 3.1 and 3.2, vs. NDS of 3.3, 7.2 and 9.1 in plants without 7E, a reduction in NDS of 2.1, 4.1 and 5.9 in the respective populations. The QTL on 7E and the Fhb1 gene augment disease resistance when combined. The effect of the QTL on 7E was greater than that on 3BS in this experiment. Data also suggest that the FHB resistance gene derived from L. elongatum is located on the long arm of 7E.     

Molecular and physical mapping of genes affecting awning in wheat

Quantitative trait loci (QTL) for three traits related to awning (awn length at the base, the middle and the top of the ear) in wheat were mapped in a doubled‐haploid line (DH) population derived from the cross between the cultivars ‘Courtot’ (awned) and ‘Chinese Spring’ (awnless) and grown in Clermont‐Ferrand, France, under natural field conditions. A molecular marker linkage map of this cross that was previously constructed based on 187 DH lines and 550 markers was used for the QTL mapping. The genome was well covered (more than 95%) and a set of anchor loci regularly spaced (one marker every 20.8 cM) was chosen for marker regression analysis. For each trait, only two consistent QTL were identified with individual effects ranging from 8.5 to 45.9% of the total phenotypic variation. These two QTL cosegregated with the genes Hd on chromosome 4A and B2 on chromosome 6B, which are known to inhibit awning. The results were confirmed using ‘Chinese Spring’ deletion lines of these two chromosomes, which have awned spikes, while ‘Chinese Spring’ is usually awnless. No quantitative trait locus was detected on chromosome 5A where the B1 awn‐inhibitor gene is located, suggesting that both ‘Courtot’ and ‘Chinese Spring’ have the same allelic constitution at this locus. The occurrence of awned speltoid spikes on the deletion lines of this chromosome suggests that ‘Chinese Spring’ and ‘Courtot’ have the dominant B1 allele, indicating that B1 alone has insufficient effect to induce complete awn inhibition.     

Different quantitative trait loci for <Emphasis Type="Italic">Fusarium</Emphasis> resistance in wheat seedlings and adult stage in the Wuhan/Nyubai wheat population

Fusarium head blight (FHB), caused primarily by Fusarium graminearum (Schwabe), is an important wheat disease. In addition to head blight, F. graminearum also causes Fusarium seedling blight (FSB) and produces the mycotoxin deoxynivalenol (DON) in the grain. The objectives of this study were: (1) to compare the relationship between resistance of wheat lines to F. graminearum in the seedlings and spikes and (2) to determine whether the quantitative trait loci (QTL) for FSB were the same as QTLs for FHB resistance and DON level reported for the same population previously (Somers et al. 2003). There was no relationship between FSB infection and FHB index or DON content across the population. A single QTL on chromosome 5B that controlled FSB resistance was identified in the population; the marker WMC75 explained 13.8% of the phenotypic variation for FSB. This value implies that there may be other QTL with minor effects present, but they were not detected in the analysis. Such a QTL on chromosome 5B was not reported previously among the QTLs associated with FHB resistance and DON level in this population. However, because of recombination, some lines in the present study have Fusarium resistance for both seedling and head blight simultaneously. For example, DH line HC 450 had the highest level of resistance to FSB and FHB and was among the ten lines with lowest DON content. This line is a good candidate to be used as a parent for future crosses in breeding for Fusarium seedling resistance, together with breeding for head blight resistance. This approach may be effective in increasing overall plant resistance to Fusarium.     

QTL mapping of net blotch resistance genes in a doubled-haploid population of six-rowed barley

Net blotch, caused by Pyrenophora teres f. teres, is a damaging foliar disease of barley worldwide. It is important to identify resistance germplasm and study their genetics. 'Chevron', a six-rowed barley used as a parent for the production of a doubled haploid (DH) population for mapping of Fusarium head blight (FHB) resistance, was also found to be resistant to net blotch. To map the resistance genes, the population was evaluated for resistance at the seedling stage in a greenhouse. The resistance data showed a two-peak distribution. Through linkage mapping, one resistance gene, tentatively called Rpt, was located on chromosome 6HS flanked by Xksua3b-Xwg719d, which was also detected by QTL mapping. This QTL explained 64% of the phenotypic variance for the resistance in this DH population. In addition, a minor QTL was found on chromosome 2HS defined by Xcdo786-Xabc156a. 'Chevron' and 'Stander' contributed the resistant alleles of Rpt and the 2HS QTL, respectively. Both QTLs together explained nearly 70% of the phenotypic variance. The markers for these QTLs are useful for marker-assisted selection of net blotch resistance in barley breeding.     

Quantitative trait loci for leafhopper (Empoasca fabae and Empoasca kraemeri) resistance and seed weight in the common bean

A population of 108 common bean recombinant inbred lines (RILs) (F_5:6‐9), derived from a leafhopper (Empoasca fabae and E. kraemeri)‐susceptible cultivar (‘Berna’) and a leafhopper‐resistant line (EMP 419) was used to identify molecular markers genetically linked to leafhopper resistance and seed weight. Bulked segregant analysis and quantitative trait analysis identified eight markers that were associated with resistance to E. fabae, and four markers that were associated with E. kraemeri resistance. Three markers were associated with resistance to both species. A partial linkage map of the bean genome was constructed. Composite interval mapping identified quantitative trait loci (QTL) for resistance to both leaf hopper species on core‐map linkage groups B1, B3 and B7. QTL for seed weight were found close to the locus controlling testa colour and an α‐phaseolin gene.     

Molecular mapping of cereal cyst nematode resistance in <Emphasis Type="Italic">Triticum monococcum</Emphasis> L. and its transfer to the genetic background of cultivated wheat

Triticum monococcum, the diploid A genome species, harbours enormous variability for resistance to biotic stresses. A spring type T. monococcum acc. 14087 was found to be resistant to Heterodera avenae (cereal cyst nematode, CCN). A recombinant inbred line population (RIL) developed by crossing this accession with a CCN susceptible T. boeoticum acc. 5088 was used for studying the inheritance and map location of the CCN resistance. Based on composite interval mapping two QTL, one each on chromosome 1AS and 2AS, were detected. The QTL on 1A, designated as Qcre.pau-1A, appeared to be a major gene with 26% contribution to the overall phenotypic variance whereas the QTL on 2A designated as Qcre.pau-2A contributed 13% to total phenotypic variation. Qcre.pau-1A is novel, being the only CCN resistance gene mapped in any ‘A’ genome species and none of the other known genes have been mapped on chromosome 1A. The QTL Qcre.pau-2A might be allelic to Cre5, a CCN resistance gene transferred from Ae. ventricosa and mapped on 2AS. The Qcre.pau-1A was transferred to cultivated wheat using T. durum cv. PBW114 as the bridging species. Selected CCN resistant F₈ lines showed introgression for the molecular markers identified to be linked with CCN resistance locus Qcre.pau-1A. Thus, this gene alone could impart complete resistance against CCN. These introgression lines can be used for marker-assisted transfer of Qcre.pau-1A to elite wheat cultivars.     

Genetic analysis of falling number in three bi‐parental common winter wheat populations

The objective of the present study was to analyse the genetic basis of falling number in three winter wheat populations. Samples for falling number determination for each population originated from at least three test environments that were free from the occurrence of preharvest sprouting at harvest time. Quantitative trait locus (QTL) analysis employing falling number values from single environments identified eight, five and three QTL in the populations Dream/Lynx, Bussard/W332‐84 and BAUB469511/Format, respectively. A major QTL common to all three populations and consistently detected in each environment mapped to the long arm of chromosome 7B. The QTL was located to a similar genomic region as the previously described major QTL for high‐isoelectric point α‐amylase content. The T1BL.1RS wheat‐rye translocation and the dwarfing gene Rht‐D1 segregating in Dream/Lynx and BAUB469511/Format were found to be important factors of falling number variation. In both populations, the presence of Rht‐D1b or the absence of T1BL.1RS increased falling number. The results indicate that late maturity α‐amylase, responsible for low falling numbers, has now been documented in German wheat germplasm.     

QTL analysis of resistance to Fusarium head blight in wheat using a 'Wangshuibai'-derived population

Fusarium head blight (FHB) is a devastating disease that reduces the yield, quality and economic value of wheat. For quantitative trait loci (QTL) analysis of resistance to FHB, F₃ plants and F_3:5 lines, derived from a ‘Wangshuibai’ (resistant)/‘Seri82’(susceptible) cross, were spray inoculated during 2001 and 2002, respectively. Artificial inoculation was carried out under field conditions. Of 420 markers, 258 amplified fragment length polymorphism and 39 simple sequence repeat (SSR) markers were mapped and yielded 44 linkage groups covering a total genetic distance of 2554 cM. QTL analysis was based on the constructed linkage map and area under the disease progress curve. The analyses revealed a QTL in the map interval Xgwm533‐Xs18/m12 on chromosome 3BS accounting for up to 17% of the phenotypic variation. In addition, a QTL was detected in the map interval Xgwm539‐Xs15/m24 on chromosome 2DL explaining up to 11% of the phenotypic variation. The QTL alleles originated from ‘Wangshuibai’ and were tagged with SSR markers. Using these SSR markers would facilitate marker‐assisted selection to improve FHB resistance in wheat.     

Identification of novel QTL for resistance to crown rot in the doubled haploid wheat population 'W21MMT70' × 'Mendos'

Crown rot (causal agent Fusarium pseudograminearum) is a fungal disease of major significance to wheat cultivation in Australia. A doubled haploid wheat population was produced from a cross between line ‘W21MMT70’, which displays partial seedling and adult plant (field) resistance to crown rot, and ‘Mendos’, which is moderately susceptible in seedling tests but partially resistant in field trials. Bulked segregant analysis (BSA) based on seedling trial data did not reveal markers for crown rot resistance. A framework map was produced consisting of 128 microsatellite markers, four phenotypic markers, and one sequence tagged site marker. To this map 331 previously screened AFLP markers were then added. Three quantitative trait loci (QTL) were identified with composite interval mapping across all of the three seedling trials conducted. These QTL are located on chromosomes 2B, 2D and 5D. The 2D and 5D QTL are inherited from the line ‘W21MMT70’, whereas the 2B QTL is inherited from ‘Mendos’. These loci are different from those associated with crown rot resistance in other wheat populations that have been examined, and may represent an opportunity for pyramiding QTL to provide more durable resistance to crown rot.     

Molecular mapping of quantitative trait loci (QTLs) controlling aluminium tolerance in bread wheat

Aluminium (Al) toxicity is a major constraint to crop productivity in acidic soils. A quantitative trait locus (QTL) analysis was performed to identify the genetic basis of Al tolerance in the wheat cultivar ‘Chinese Spring’. A nutrient solution culture approach was undertaken with the root tolerance index (RTI) and hematoxylin staining method as parameters to assess the Al tolerance. Using a set of D genome introgression lines, a major Al tolerance QTL was located on chromosome arm 4DL, explaining 31% of the phenotypic variance present in the population. A doubled haploid population was used to map a second major Al tolerance QTL to chromosome arm 3BL. This major QTL (Qalt _CS .ipk-3B) in ‘Chinese Spring’ accounted for 49% of the phenotypic variation. Linkage of this latter QTL to SSR markers opens the possibility to apply marker-assisted selection (MAS) and pyramiding of this new QTL to improve the Al tolerance of wheat cultivars in breeding programmes.     

Genetic analysis of salt tolerance in a recombinant inbred population of wheat (Triticum aestivum L.)

A population of 114 recombinant inbred lines (RILs), derived from the cross Opata85 × W7984, was used to genetically analyze the response of wheat to salt stress. This analysis resulted in the identification of 47 QTL mapping to all wheat chromosomes except 1B, 1D, 4B, 5D and 7D. Of these QTL, 10 were effective during the germination stage, and 37 at the seedling stage. Many of the traits related to salt tolerance mapped to common chromosome intervals, such as Xglk683–Xcdo460 on chromosome 3A, Xfbb168–Xbcd147 on chromosome 3B, Xcdo1081–Xfbb226 on chromosome 4DL and Xpsr106–Xfbb283 on chromosome 6DL. QTL located in the interval Xcdo1081–Xfbb226 (chromosome 4DL) were effective during the germination stage, whereas those in the interval Xfbb231.1–Xmwg916 (chromosome 6DL) were relevant to the seedling stage. The QTL in the intervals Xglk683–Xcdo460 (chromosome 3AS) and Xfbb168–Xbcd147 (chromosome 3BL) were effective at both the germination and seedling stages.