Long Arm Of Chromosome 5B Research Articles

A Novel Source of Resistance in Wheat to Pyrenophora tritici-repentis 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.

Chromosome pairing in durum wheat haploids with and without ph1b of bread wheat

Durum or macaroni wheat (Triticum turgidum L., 2n = 4x = 28; AABB) is an allotetraploid with two related genomes, AA and BB, each with seven pairs of homologous chromosomes. Although the corresponding chromosomes of the two genomes are potentially capable of pairing with one another, the Ph1 (Pairing homoeologous) gene in the long arm of chromosome 5B permits pairing only between homologous partners. As a result of this Ph1-exercised disciplinary control, durum wheat and its successor, bread wheat (Triticum aestivum L., 2n = 6x = 42; AABBDD) show diploid-like chromosome pairing and hence disomic inheritance. The Ph mutants in the form of deletions are available in bread wheat (ph1b) and durum wheat (ph1c). Thus, ph1b-haploids of bread wheat and ph1c-haploids of durum wheat show extensive homoeologous pairing that has been shown by us and several others. Here we study the effect of ph1b allele of bread wheat on chromosome pairing in durum haploids, whereas we studied earlier the effect of ph1c allele in durum haploids that we synthesized. In durum wheat, the ph1b-haploids show much higher (49.4% of complement) pairing than the ph1c-haploids (38.6% of complement).

Genetics and molecular mapping of resistance to necrosis inducing race 5 of Pyrenophora tritici-repentis in tetraploid wheat

Race 5 of Pyrenophora tritici-repentis, causal agent of tan spot, induces two distinct symptoms, necrosis and chlorosis in susceptible tetraploid and hexaploid wheat, respectively. This study was conducted under controlled environmental conditions to determine the inheritance of resistance to P. tritici-repentis, race 5, in a tetraploid wheat population and to map the resistance genes. Additionally, the relationship between the resistance genes effective against necrosis inducing races 3 and 5 in tetraploid wheat was determined. A population of 98 recombinant-inbred lines (RIL) was developed from a cross between the resistant genotype Triticum turgidum # 283 (PI352519) and the susceptible durum cultivar Coulter. This RIL population was screened individually with race 3 and race 5 and molecular mapping of the resistance gene(s) in this population was conducted. Additionally, the F2 and F4:5 generations of this population were screened with race 5 to determine the genetic control of resistance. Plants were inoculated at the two-leaf stage and disease reaction was assessed based on 1 to 5 lesion-type rating scale eight days after inoculation. Segregation 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 5. Analysis of the mapping data of the T. turgidum # 283/Coulter RIL population indicate that a major gene, designated tsn5, controlling resistance to race 5 is located on the long arm of chromosome 3B. The tsn5 gene is 8.3 cM proximal to the gene tsn2 that controls resistance to necrosis induced by race 3.

Discrimination of the Triticum aestivum-T. timopheevii introgression lines using PCR-based molecular markers

In order to determine the fragment size of Triticum timopheevii chromosome segments introduced into wheat background and physically map the Pm6 gene, a total of 72 primers (including SSR and STS primers) were used to analyze the eight introduced introgression lines containing Pm6 gene. Referring to the available mapping information of the analyzed markers on chromosome 2B, Pm6 was physically located in distal part of the long arm of chromosome 2B at the region of Bin 2BL-6. The introgressed fragment sizes of the chromosome 2G in different introgression lines was determined to be as follow (from short to long): IGV1-465<IGV1-464<IGV1-463<IGV1-468<(IGV1-448,IGV1-458)<IGV1-474< IGV1-466. The results were coincide with the RFLP results and further confirmed that line IGV1-465 contained the minimum introgression segment. Using the 10 polymorphism PCR markers identified in the present research, it is feasible to differentiate seven introgression lines. This information will be helpful for marker assistant identification of these lines in wheat breeding program and for further isolation of the Pm6 gene.

Discovery and Mapping of Wheat Ph1 Suppressors

Pairing between wheat (Triticum turgidum and T. aestivum) homeologous chromosomes is prevented by the expression of the Ph1 locus on the long arm of chromosome 5B. The genome of Aegilops speltoides suppresses Ph1 expression in wheat x Ae. speltoides hybrids. Suppressors with major effects were mapped as Mendelian loci on the long arms of Ae. speltoides chromosomes 3S and 7S. The chromosome 3S locus was designated Su1-Ph1 and the chromosome 7S locus was designated Su2-Ph1. A QTL with a minor effect was mapped on the short arm of chromosome 5S and was designated QPh.ucd-5S. The expression of Su1-Ph1 and Su2-Ph1 increased homeologous chromosome pairing in T. aestivum x Ae. speltoides hybrids by 8.4 and 5.8 chiasmata/cell, respectively. Su1-Ph1 was completely epistatic to Su2-Ph1, and the two genes acting together increased homeologous chromosome pairing in T. aestivum x Ae. speltoides hybrids to the same level as Su1-Ph1 acting alone. QPh.ucd-5S expression increased homeologous chromosome pairing by 1.6 chiasmata/cell in T. aestivum x Ae. speltoides hybrids and was additive to the expression of Su2-Ph1. It is hypothesized that the products of Su1-Ph1 and Su2-Ph1 affect pairing between homeologous chromosomes by regulating the expression of Ph1 but the product of QPh.ucd-5S may primarily regulate recombination between homologous chromosomes.

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

ABSTRACT 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 F(2) generation and of the F(4:5) and F(6:7) families indicated that a single recessive gene controlled resistance to necrosis induced by race 3 in the cross studied.

SNP‐Based Improvement of a Microsatellite Marker Associated with Karnal Bunt Resistance in Wheat

Marker‐assisted selection (MAS) has become the technology of choice for introgressing important traits with indistinct phenotypes into agronomically elite cultivars. Karnal bunt (KB, causal agent Tilletia indica Mitra) is an economically important fungal pathogen of wheat (Triticum aestivum L.) which has caused economic losses in the USA since it was first reported in 1996. To protect U.S. wheat from this emerging disease and the losses incurred from export quarantines, genetic sources of resistance are needed by breeders to improve U.S. germplasm. Resistance to KB is difficult to score phenotypically, making MAS an ideal choice for deploying this trait into U.S. wheat. Here we describe the conversion of a codominant microsatellite marker, Xgwm538, associated with a quantitative trait locus (QTL) for KB resistance into a single nucleotide polymorphism (SNP) based marker. The SNP marker was developed to improve gel‐based resolution and amplification consistency. The gwm538 primers amplify three fragments in the KB resistant line HD29: 137‐, 147‐, and a 152‐bp fragment that maps to the long arm of chromosome 4B and is linked to the KB QTL. By cloning and sequencing all three fragments, we were able to exploit a SNP and design a new primer to selectively amplify the 152‐bp fragment of interest (gwm538snp). Amplification consistency is improved with gwm538snp since the amplification of competing nontarget fragments is eliminated, and ambiguity is reduced since heterozygous plants are easily identified among backcross progeny.

Gene evolution at the ends of wheat chromosomes

Wheat ESTs mapped to deletion bins in the distal 42% of the long arm of chromosome 4B (4BL) were ordered in silico based on blastn homology against rice pseudochromosome 3. The ESTs spanned 29 cM on the short arm of rice chromosome 3, which is known to be syntenic to long arms of group-4 chromosomes of wheat. Fine-scale deletion-bin and genetic mapping revealed that 83% of ESTs were syntenic between wheat and rice, a far higher level of synteny than previously reported, and 6% were nonsyntenic (not located on rice chromosome 3). One inversion spanning a 5-cM region in rice and three deletion bins in wheat was identified. The remaining 11% of wheat ESTs showed no sequence homology in rice and mapped to the terminal 5% of the wheat chromosome 4BL. In this region, 27% of ESTs were duplicated, and it accounted for 70% of the recombination in the 4BL arm. Globally in wheat, no sequence homology ESTs mapped to the terminal bins, and ESTs rarely mapped to interstitial chromosomal regions known to be recombination hot spots. The wheat-rice comparative genomics analysis indicated that gene evolution occurs preferentially at the ends of chromosomes, driven by duplication and divergence associated with high rates of recombination.

Identification of quantitative trait loci for race-nonspecific resistance to tan spot in wheat

Tan spot, caused by Pyrenophora tritici-repentis (Ptr), is an economically important foliar disease in the major wheat growing areas throughout the world. Multiple races of the pathogen have been characterized based on their ability to cause necrosis and/or chlorosis on differential wheat lines. In this research, we evaluated a population of recombinant inbred lines derived from a cross between the common wheat varieties Grandin and BR34 for reaction to tan spot caused by Ptr races 1-3 and 5. Composite interval mapping revealed QTLs on the short arm of chromosome 1B and the long arm of chromosome 3B that were significantly associated with resistance to all four races. The effects of the two QTLs varied for the different races. The 1B QTL explained from 13% to 29% of the phenotypic variation, whereas the 3B QTL explained from 13% to 41% of the variation. Additional minor QTLs were detected but not associated with resistance to all races. The host-selective toxin Ptr ToxA, which is produced by races 1 and 2, was not a significant factor in the development of disease in this population. The race-nonspecific resistance derived from BR34 may take precedence over the gene-for-gene interaction known to be associated with the wheat-Ptr system.

Genetic analysis of durable resistance to yellow rust in bread wheat

Yellow rust, caused by Puccinia striiformis, is one of the most damaging diseases affecting bread wheat in temperate regions. Although resistance to yellow rust is frequently overcome by new virulent races, a durable form of resistance in the French bread wheat Camp Remy (CR) has remained effective since its introduction in 1980. We used 217 F7 recombinant inbred lines (RILs) derived from the cross between CR and the susceptible cultivar Recital to identify and map quantitative trait loci (QTLs) involved in durable yellow rust resistance. Six significant QTLs that were stable over a 4-year period were detected. Two QTLs, denoted QYr.inra-2DS and QYr.inra-5BL.2, were located on the short arm of chromosome 2D and the long arm of chromosome 5B, respectively. Each explained on average 25-35% of the observed phenotypic variation and were probably inherited from Cappelle Desprez, a parent of CR that confers durable adult plant resistance to yellow rust. QYr.inra-2DS probably corresponds to the Yr16 gene. The most consistent QTL, designated QYr.inra-2BL, was located on the centromeric region of chromosome 2B and explained 61% of the phenotypic variation in 2003. This QTL was responsible for seedling-stage resistance and may correspond to a cluster of genes, including Yr7. The remaining QTLs were mapped to the short arm of chromosome 2B (R2=22-70%) and to the long arm of chromosomes 2A (R2=0.20-0.40) and 5B (R2=0.18-0.26). This specific combination of seedling and adult plant resistance genes found in CR and CD may constitute the key to their durable resistance against yellow rust.

PCR Markers for Triticum speltoides Leaf Rust Resistance Gene Lr51 and Their Use to Develop Isogenic Hard Red Spring Wheat Lines

New leaf rust resistance genes are needed in wheat (Triticum aestivum L.) to provide additional sources of resistance to the highly variable and dynamic leaf rust pathogen Puccinia triticina Eriks. Leaf rust resistance gene Lr51, located within a segment of Triticum speltoides Taush chromosome 1S translocated to the long arm of chromosome 1B of bread wheat, is resistant to the current predominant races of leaf rust in the USA. The objectives of this study were to determine the genetic length of the translocated 1S segment, develop a PCR marker for Lr51, and use this marker to generate isogenic lines for this gene. Characterization of two translocation lines (F‐7‐3 and F‐7‐12) with 10 molecular markers indicated that F‐7‐3 has an interstitial T. speltoides chromosome segment of 14 to 32 cM long including loci XAga7 and Xmwg710, whereas line F‐7‐12 has a complex series of translocations among chromosomes of homeologous group 1. On the basis of the DNA sequence of the A, B, D, and S alleles of the XAga7 locus, we designed a cleavage amplified polymorphic sequence (CAPS) marker for the S genome allele. Primers S30‐13L and AGA7‐759R preferentially amplified the XAga7 1S (819 bp) and 1B alleles (783 bp). These amplification products can be separated in agarose gels after digestion with PstI or BamHI restriction enzymes. This CAPS marker was validated in a collection of 32 common wheat cultivars and was used to develop three pairs of hard red spring isogenic lines from the donor parent F‐7‐3. These isogenic lines will be valuable for future assessment of the effect of this chromosome introgression on agronomic performance and end‐use quality.

Mapping of QTLs prolonging the latent period of Puccinia triticina infection in wheat

Slow rusting is considered a crucial component of durable resistance to wheat leaf rust caused by Puccinia triticina and is often expressed in the form of a prolonged latent period. Selection for a longer latent period is considered an effective approach to developing wheat cultivars with improved durable resistance to leaf rust. A recombinant inbred line (RIL) population derived from CI 13227 (long latent period) x Suwon 92 (short latent period) was phenotyped for latent period in two greenhouse experiments in separate years, and amplified fragment length polymorphism (AFLP) and simple sequence repeat (SSR) markers were analyzed in the same population. Among the RILs, the frequency distribution for latent period was continuous, and latent period was highly correlated between years (r=0.94, P<0.0001). A quantitative trait locus (QTL) prolonging the latent period of P. triticina, designated as QLrlp.osu-2DS, explained 42.8% and 54.5% of the phenotypic and genetic variance in the two experiments, respectively. QLrlp.osu-2DS was mapped on the distal region of chromosome 2DS. Two other QTLs for latent period, QLrlp.osu-2B and QLrlp.osu-7BL, were localized on chromosome 2B and the long arm of chromosome 7B, respectively. Multiple regression analysis showed that these three QTLs collectively explained 58.0% and 73.8% of the phenotypic and genetic variance over two experiments, respectively. Fourteen RILs that carried all three alleles for long latent period at three AFLP loci flanking QLrlp.osu-2DS, QLrlp.osu-2B, and QLrlp.osu-7BL had a mean latent period of 12.5 days, whereas 13 RILs without any long-latent-period alleles at the corresponding loci had a mean latent period of 7.4 days. Three SSR markers closely linked to these QTLs have potential to be applied in marker-assisted selection for prolonged latent period in wheat.

Cytological and microsatellite mapping of the genes determining liguleless phenotype in durum wheat

Liguleless phenotypes of wheat lack ligule and auricle structures on all leaves of the plant. Two recessive genes principally control the liguleless character in tetraploid wheat. The F2 progenies of k17769 (liguleless mutant)/Triticum dicoccoides and k17769/T. dicoccum segregated in a 15:1 ratio, whereas the F2 progenies of k17769/T. durum and k17769/T. turgidum segregated in a 3:1 ratio. A new gene, lg 3, was found on chromosome 2A. Segregation of F2 progenies between k17769 and chromosome substitution lines for homoeologous group 2 chromosomes suggested that the liguleless genotype had occurred by mutation at the lg 3 locus on chromosome 2A, and then by mutation at the lg 1 locus on chromosome 2B, in the process of domestication of tetraploid wheat. The gene (lg 1) was linked to Tc 2 (11.9 cM), which determines phenol colour reaction of kernels, on the long arm of chromosome 2B. The distance of lg 1 to the centromere was found to be 60.4 cM, and microsatellite mapping established the gene order, centromere – Xgwm382 – Xgwm619 – Tc 2 – lg 1 on the long arm of chromosome 2B.

A chromosome-specific sequence common to the B genome of polyploid wheat and Aegilops searsii

A low-copy, non-coding chromosome-specific DNA sequence, isolated from common wheat, was physically mapped to the distal 19% region of the long arm of chromosome 3B (3BL) of common wheat. This sequence, designated WPG118, was then characterized by Southern hybridization, PCR amplification and sequence comparison using a large collection of polyploid wheats and diploid Triticum and Aegilops species. The data show that the sequence exists in all polyploid wheats containing the B genome and absent from those containing the G genome. At the diploid level, it exists only in Ae. searsii, a diploid species of section Sitopsis, and not in other diploids including Ae. speltoides, the closest extant relative to the donor of the B genome of polyploid wheat. This finding may support the hypothesis that the B-genome of polyploid wheat is of a polyphyletic origin, i.e. it is a recombined genome derived from two or more diploid Aegilops species.

Detection of QTLs for Stagonospora glume blotch resistance in Swiss winter wheat.

Stagonospora nodorum is the causal agent of the Stagonospora glume blotch disease in hexaploid wheat. The Swiss winter bread wheat cv. 'Arina' has a highly effective, durable and quantitative glume blotch resistance. We studied 240 single seed descent (SSD)-derived lines of an 'Arina x Forno' F(5:7) population to identify and map quantitative trait loci (QTLs) for glume blotch resistance under natural infestation. Using composite interval mapping (CIM) and LOD>4.5, we detected two chromosomal regions on chromosome arms 3BS and 4BL which were specifically associated with glume blotch resistance. These identified QTLs were designated QSng.sfr-3BS and QSng.sfr-4BL, respectively. QSng.sfr-3BS peaked at the locus Xgwm389 in the telomeric region of the short arm of chromosome 3B and explained 31.2% of the observed phenotypic variance for the resistance within the population. The responsible QSng.sfr-3BS allele originated from the resistant parent 'Arina'. The QTL QSng.sfr-4BL (19.1%) mapped to chromosome arm 4BL ('Forno' allele) very close to two known genes, TaMlo and a catalase ( Cat). Both QTL alleles combined could enhance the resistance level by about 50%. Additionally, they showed significant epistatic effects (4.4%). We found PCR-based microsatellite markers closely linked to QSng.sfr-3BS (gwm389) and QSng.sfr-4BL (gwm251) which make marker-assisted selection (MAS) for Stagonospora glume blotch resistance feasible. We also found one resistance QTL, QSng.sfr-5BL, on the long arm of chromosome 5B which overlapped with QTLs for plant height as well as heading time.

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

AbstractAn 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.

WAG, a wheat AGAMOUS homolog, is associated with development of pistil-like stamens in alloplasmic wheats

Pistillody, homeotic transformation of stamens into pistil-like structures, has been reported in cytoplasmic substitution (alloplasmic) lines of common wheat (Triticum aestivum) with Aegilops crassa cytoplasm. The induction of pistillody is suppressed by the Rfd1 gene detected on the long arm of chromosome 7B in wheat cultivar 'Chinese Spring' (CS). Because of the absence of Rfd1, the alloplasmic line CS ditelosomic 7BS [(cr)-CSdt7BS] lacking the long arm of chromosome 7B exhibits pistillody in all florets, whereas the euplasmic CS ditelosomic 7BS (CSdt7BS) with normal cytoplasm forms normal stamens. To study the molecular mechanism of pistillody caused by nuclear-cytoplasm interaction in alloplasmic wheat, we cloned and characterized a wheat AGAMOUS homolog, WAG. The WAG gene copy number in the wheat genome was estimated at three, located on the homoeologous group 1 chromosomes. Northern blot analysis with a normal wheat line revealed that the transcription level of WAG was lower in young spikes and increased during spike development. The highest expression was observed in spikes at the booting to heading stage. The 1.1 kb WAG transcript accumulated in both the reproductive (pistil and stamen) and non-reproductive (palea and lemma) portions of spikes at the heading stage, whereas an extra transcript of different molecular size (1.3 kb) was observed in pistil-like stamens of line (cr)-CSdt7BS as well as in pistils of CSdt7BS and (cr)-CSdt7BS. These results suggest that the product of the 1.3 kb WAG transcript is involved in pistil development and is associated with pistillody caused by a nuclear-cytoplasm interaction in alloplasmic wheat.

Mapping of chlorina mutant genes on the long arm of homoeologous group 7 chromosomes in common wheat with partial deletion lines

The chlorophyll a:b ratio of chlorina mutants is much higher than that of wild type plants. Physical mapping of the chlorina mutant loci (cn-A1, cn-B1 and cn-D1) of common wheat (Triticum aestivum L.) and durum wheat (T. turgidum L.) was carried out with partial deletion lines of Chinese Spring(CS) of the long arms of homoeologous group7 chromosomes. F1 plants of partial deletion lines with near-isogenic lines (ANK-32A and ANK-32B) of the spring bread wheat Novosibirskaya 67 and a near-isogenicline of durum wheat LD222, ANW-7B were evaluated for chlorophyll a:b ratio of the leaves. Hemizygous and heterozygous plants were more easily distinguished by chlorophyll a:b ratio than by visual observation. The dose effects of the chlorina loci on chlorophyll a:b ratio were also confirmed. The position of the allele on the chromosome was localized by fraction length, the comparative values between whole chromosome and partially deleted chromosome. The locus cn-A1 was localized on the region of 83% distal from the centromere on the long arm of chromosome 7A, cn-B1 locus was localized on the region between 69% and 78% distal from the centromere on the long arm of chromosome 7B, and cn-D1 locus was localized on the region between 76% and 77% distal from the centromere on the long arm of chromosome 7D. We consider the map derived by deletion mapping is more accurate than the map calculated from recombination frequency.

Mapping of a resistance gene effective against Karnal bunt pathogen of wheat.

A set of 130 wheat recombinant inbred lines (RILs) developed from a cross between parents susceptible (WL711) and resistant (HD29) to Karnal bunt (caused by Tilletia indica), were screened for 3 years with the pathogen populations prevalent in northern India. When 90 simple sequence repeats (SSRs) and 81 amplified fragment length polymorphism (AFLP) loci were mapped on the RILs, markers on chromosomes 2A, 4B and 7B accounted collectively for about one-third of the variation in the disease reaction. The genomic region of largest effect, identified on the long arm of chromosome 4B, reduced Karnal bunt disease by half in three different experiments and accounted for up to 25% of the phenotypic variation for KB reaction. A closely linked SSR marker, GWM538, may be useful in marker-assisted selection for Karnal bunt resistance in wheat.

Microsatellite marker for yellow rust resistance gene Yr5 in wheat introgressed from spelt wheat

AbstractYellow rust of wheat caused by Puccinia striiformis f sp. tritici has been periodically epidemic and severely damaged wheat production in China and throughout the world. Breeding for resistant cultivars has been proved to be an effective way to resolve the problem. A yellow rust resistance gene, Yr5, derived from Triticum spelta shows immunity or high resistance to the most popular isolates Tiaozhong 30 and 31 in China. Establishment of DNA markers for the Yr5 gene will facilitate marker‐assisted selection and gene pyramiding in the breeding programme. Since the Yr5 gene was cytologically located on the long arm of chromosome 2B, By33, the donor of Yr5, was crossed and backcrossed with the susceptible line 441, and BC3F2 and BC3F3 segregating populations were screened for polymorphism by using 11 microsatellite primers mapped on chromosome 2B. A marker, Xgwm501‐195 bp/160 bp, was found to be linked to Yr5, with a genetic distance of 10.5‐13.3 cM.