Race-specific Resistance Genes Research Articles

Molecular mapping and intra-cluster recombination between anthracnose race-specific resistance genes in the common bean differential cultivars Mexico 222 and Widusa

Resistance to races 19, 31, 38, 65, 73, 102, and 449, of the pathogenic fungus Colletotrichum lindemuthianum (anthracnose) was evaluated in F(3) families derived from the cross between the anthracnose differential bean cultivars Mexico 222 (resistant to races 19, 31, and 38) and Widusa (resistant to races 38, 65, 73, 102, and 449). Molecular marker analyses were carried out in the corresponding F(2) individuals in order to identify the genes for anthracnose resistance present in these two differential cultivars. The results of the combined segregation indicate that the resistance to anthracnose races 19, 31, and 38, present in Mexico 222, is conferred by single dominant race-specific genes organized in a cluster located in B4 linkage group, corresponding to the previously described Co-3/Co-9 locus. The resistance to anthracnose races 65, 73, 102, and 449, present in Widusa, is conferred by a dominant gene (or genes) representing a different haplotype of the same Co-3/Co-9 cluster. A single dominant gene located in a position independent from cluster Co-3/Co-9 (probably at the Co-1 locus) confers specific resistance to race 38 in Widusa. Recombinants for closely linked resistance specificities belonging to the Co-3/Co-9 cluster have been detected. The possibility of pyramiding race-specific resistance genes by means of intra-cluster recombination, and its potential use in plant breeding, is indicated.

Quantitative Trait Loci in Bread Wheat (Triticum Aestivum L.) Associated with Resistance to Stripe Rust

ABSTRACTStripe rust is an important wheat disease worldwide and resistance to stripe rust is often not controlled by race-specific resistance genes. To identify quantitative trait loci (QTL) affecting quantitative resistance to stripe rust, 329 F2:3 families from a cross between highly resistant winter type cv. MV17 and highly susceptible spring type local cv. Bolani were used. The population was evaluated for adult plant resistance to pathotype 134E134A+ of Puccinia striiformis, in the field condition and area under the disease progress curve (AUDPC) was calculated. Fifty six polymorphic SSR markers between parental genotypes were screened in the population and linkage map was constructed using these markers. Based on composite interval mapping (CIM) 14 regions on nine (4A, 1B, 2B, 3B, 4B, 5B, 6B, 2D and 7D) out of the 21 wheat chromosomes were significantly associated with AUDPC. The effect of QTLs varied from 0.01 to 8.00% giving an aggregate effect of 34.3% for AUDPC. Leaf tip necrosis (LTN) was also recorded as presence and absence and the phenotype was used as a dominant Mendelian morphologic marker. Linkage analysis revealed association between LTN and Xbarc352 SSR marker on chromosome 7D.

Accumulations of genes for durable resistance to wheat leaf rust pathogen

The individual use of single race-specific resistance genes with major phenotypic effects has rarely provided lasting resistance. However, breeding and combining or pyramiding of resistance genes into individual cultivars has had considerable success, particularly in situation where the pathogen does not reproduce sexually, as in the case of wheat leaf rust pathogen. Within international leaf rust of wheat investigations it was necessary, to create by breeding new resistant wheat lines to Puccinia recondita tritici for differentiation of pathogen population, as well as for sources of resistance in European-Mediterranean regions. In the beginning 18 donors of resistance had been selected after an extensive screening test of several International Rust Nurseries, to be crosses with recur- rent parents varieties Princ and Starke. These tests proved that in those lines were present new resistant genes. Eighth genetically different hybrids of the first back-cross had been selected and tested in the seedling stage with three international pathogen cultures (YU-13-19-1; H-13-9-1 and C2-13-Ar-3). Considerable influence of recurrent parent to the number of resistant genes in donors used was demonstrated. On the other side, it was established considerable influence of the pathogen culture to the number of resistant genes in donors used. The same crossing combinations tested with one pathogen culture results in presence of two resistance genes, but with another culture three or one resistant gene. In order to enhancement resistance and pyramiding genes in these hybrids, eight selected the most interesting lines have been crossed with only effective isogenic containing the strong genes Lr9, Lr19 and Lr24.The genetic analysis of twenty two crossing combinations have been realized by testing with three pathotypes of Puccinia recondita tritici ( Bg.s. 12/89; Is.w 8/89 and Chl.w. 14/89). On the base of different segregation ratios of all crossing combinations it was proved that no one of the resistant donors contained the strong resistant genes used. It means that our hybrid lines contained resistant genes from the donors and in addition three strong resistant genes Lr9, Lr19 and Lr24.

Mapping quantitative trait loci controlling common bunt resistance in a doubled haploid population derived from the spring wheat cross RL4452 × AC Domain

Wheat resistance to common bunt is a highly desirable trait for environmentally friendly grain grade protection. Valuable breeding achievements have been made to develop wheat varieties with enhanced resistance to the disease, and mapping of race-specific resistance genes has been reported. However, less is known of the chromosomal regions that control non-race specific resistance to common bunt. In this study, we have characterized a segregating population of 185 doubled haploid spring wheat lines derived from the cross RL4452 × AC Domain. Reactions to a mixture of common bunt races were assessed under field simulated spring-sown conditions in greenhouses in two locations over 2 years. A total 369 polymorphic maker loci including 356 microsatellite loci, five expressed sequences tag (ESTs), and eight genes were used to develop a linkage map. Quantitative trait loci (QTL) analysis using composite interval mapping detected three QTLs associated with common bunt resistance, of which two were located on chromosome 1B and one on chromosome 7A. AC Domain alleles contributed the common bunt resistance at all three QTLs. Usefulness of gene tagging within the identified chromosomal regions for common bunt resistance breeding is discussed.

Identification of new sources of bacterial blight (Xanthomonas oryzae pv. oryzae) resistance in wild Oryza species and O. glaberrima

Bacterial blight (BB) of rice is a widespread disease in tropical Asia, contained largely through the deployment of race-specific resistance genes. Although more than 25 BB resistance genes have been identified, none are effective individually against all the pathotypes prevalent in north-western India. The response of a set of 327 accessions of 13 wildOryzaspecies and cultivated African rice,O.glaberrima, was evaluated to infection with seven pathotypes ofXanthomonas oryzaepv.oryzaeover a period of 3–4 years. Of these, 67 were resistant or moderately resistant to all pathotypes. These comprised 13 accessions ofO.glaberrima, 5 ofO. barthii, 10 ofO.rufipogon, 4 ofO.longistaminata, 22 ofO.nivara, 6 ofO.officinalis, 2 ofO.rhizomatisand 5 ofO.minuta. Inheritance studies, molecular mapping and transfer of some of these genes intoO.sativassp.indicaare in progress.

Discovery and genotyping of high‐throughput SNP markers for crown rust resistance gene Pc94 in cultivated oat

AbstractCrown rust caused by Puccinia coronata f. sp. avenae Eriks is a serious problem for oat production worldwide and pyramiding multiple resistance genes into new cultivars is a key objective of breeders. Many race specific resistance genes have been mapped and markers that are closely linked to them have been identified. However, the use of these markers in oat breeding practice has been limited due to the economics of marker assisted selection (MAS) deployment. Single nucleotide polymorphism (SNP) markers have been demonstrated to have a high‐throughput capability with relatively low cost and numerous semi‐automated SNP scoring platforms exist. Gene Pc94 has remained highly effective since it was first tested on the Canadian crown rust populations in 1993 and is one of the few effective genes available in Western Canada. In the present study, PCR products were amplified using primers derived from sequences of amplified fragment length polymorphism bands which have been shown to be linked to Pc94. Genomic DNA from genotypes, with and without the Pc94 gene, were used as the PCR templates. By comparative sequence alignment amongst the PCR fragments, many putative SNP sites were identified. From these sites, four SNP sites were selected and validated by the single base extension method. One SNP site, Pc94‐SNP1a, was tested on two F2:3 populations segregating for the resistance gene. The map distances between the SNP marker and Pc94 were 2.1 and 5.4 cM in the two different populations. Various oat cultivars and germplasm lines were also tested for a wider application of the SNP marker. Fluorescent technology and capillary electrophoresis allowed for the semi‐automated, fairly high‐throughput scoring of the SNP markers.

Genetics and molecular mapping of genes for race-specific all-stage resistance and non-race-specific high-temperature adult-plant resistance to stripe rust in spring wheat cultivar Alpowa

Stripe rust, caused by Puccinia striiformis f. sp. tritici, is one of the most widespread and destructive wheat diseases worldwide. Growing resistant cultivars is the preferred control of the disease. The spring wheat cultivar 'Alpowa' has both race-specific, all-stage resistance and non-race-specific, high-temperature adult-plant (HTAP) resistances to stripe rust. To identify genes for the stripe rust resistances, Alpowa was crossed with 'Avocet Susceptible' (AVS). Seedlings of the parents, and F(1), F(2) and F(3) progeny were tested with races PST-1 and PST-21 of P. striiformis f. sp. tritici under controlled greenhouse conditions. Alpowa has a single partially dominant gene, designated as YrAlp, conferring all-stage resistance. Resistance gene analog polymorphism (RGAP) and simple sequence repeat (SSR) techniques were used to identify molecular markers linked to YrAlp. A linkage group of five RGAP markers and two SSR markers was constructed for YrAlp using 136 F(3) lines. Amplification of a set of nulli-tetrasomic Chinese Spring lines with RGAP markers Xwgp47 and Xwgp48 and the two SSR markers indicated that YrAlp is located on the short arm of chromosome 1B. To map quantitative trait loci (QTLs) for the non-race-specific HTAP resistance, the parents and 136 F(3) lines were tested at two sites near Pullman and one site near Mount Vernon, Washington, under naturally infected conditions. A major HTAP QTL was consistently detected across environments and was located on chromosome 7BL. Because of its chromosomal location and the non-race-specific nature of the HTAP resistance, this gene is different from previously described genes for adult-plant resistance, and is therefore designated Yr39. The gene contributed to 64.2% of the total variation of relative area under disease progress curve (AUDPC) data and 59.1% of the total variation of infection type data recorded at the heading-flowering stages. Two RGAP markers, Xwgp36 and Xwgp45 with the highest R (2) values were closely linked to Yr39, should be useful for incorporation of the non-race-specific resistance gene into new cultivars and for combining Yr39 with other genes for durable and high-level resistance.

Wheat leaf and stem rust in the United States

Leaf rust, caused by Puccinia triticina, is a common and widespread disease of wheat in the US. On an annual basis, over 50 races of the leaf rust fungus are detected. There are at least 5 major groups of genetically distinct P. triticina isolates in the US based on allelic variation at microsatellite loci. Distinct regional race populations of P. triticina are found in the US, due to the widespread use of race-specific leaf rust resistance (Lr) genes in different market classes of wheat. In the south-eastern States where soft red winter wheats are grown, races with virulence to Lr9, Lr11, and Lr18 are predominant. In the southern Great Plains region where hard red winter wheats are grown, races with virulence to genes Lr9, Lr17, Lr24, and Lr26 are common. In the northern Great Plains region where hard red spring wheats are grown, races with virulence to Lr2a and Lr16 are common. Due to the wide dispersal of P. triticina, some races are found in all regions of the US. Highly effective durable resistance to leaf rust has been difficult to achieve due to the high degree of virulence variation in the P. triticina population and the rapid selection of races with virulence to effective Lr genes in wheat cultivars. Hard red spring wheat cultivars with genes Lr16, Lr23, and Lr34 have been highly resistant for more than 10 years in Minnesota and the Dakotas. Stem rust, caused by P. graminis f. sp. tritici, has not been a common disease of wheat in the US since the last major epidemics in the 1950s. The low levels of stem rust infections in the US can be attributed to the increasing use of highly resistant winter and spring wheat cultivars, which has greatly reduced the overall level of stem rust urediniospores. Eradication of the alternate host, Berberis vulgaris, has reduced the number of races and slowed the emergence of new races. Resistance genes Sr2, Sr6, Sr17, Sr24, Sr31, Sr36, and SrTmp are common in the winter wheats. Genes Sr6, Sr9b, Sr11, and Sr17 are common in the spring wheats. Spring wheat cultivars may also have adult plant stem rust resistance derived from cv. Thatcher. Many of the winter and spring wheats are susceptible to the new stem rust race from East Africa; however, cultivars with resistance to this race can be found in each of the major wheat classes.

Genetic mapping of quantitative resistance to race 5 of Pseudomonas syringae pv. phaseolicola in common bean

Halo-blight is an important worldwide bacterial disease of common bean (Phaseolus vulgaris L.) caused by Pseudomonas syringae pv. phaseolicola. Nine races of the pathogen and five race-specific resistance genes have been previously described. However, a quantitative response to this pathogen has also been described. The objective of this study was to identify halo-blight resistance loci linked to molecular markers that could be used in resistance breeding. Chromosomal regions related to race 5 halo-blight resistance were localized on a genetic map of RAPD and AFLP molecular markers and constructed by the analysis of a “Jules” × “Canela” F2 progeny. “Jules” shows quantitative resistance to halo-blight and “Canela” is a very appreciated but susceptible Spanish bean landrace. Two QTL for resistance to halo-blight were mapped in two linkage groups. There were four large groups, with 14–22 molecular markers each, five with 4–8 markers each, and three with 2 or 3 markers each.

Molecular Characterization of a Powdery Mildew Resistance Gene in Wheat Cultivar Suwon 92

ABSTRACT Powdery mildew, caused by Blumeria graminis f. sp tritici, is an important foliar disease of wheat worldwide. Pyramiding race-specific genes into a single cultivar and combining race-specific resistance genes with durable resistance genes are the preferred strategies to improve the durability of powdery mildew resistance. The objectives of this study were to characterize a powdery mildew resistance gene in Suwon 92 and identify gene-specific or tightly linked molecular markers for marker-assisted selection (MAS). A population of recombinant inbred lines (RILs) was derived by single seed descent from a cross between Suwon 92 and a susceptible cultivar, CI 13227. The RILs were screened for adult-plant infection type of powdery mildew and characterized with amplified fragment length polymorphism (AFLP) and simple sequence repeat (SSR) markers. The linked markers explained 41.3 to 69.2% of the phenotypic variances measured in 2 years. A morphological marker, hairy glume, was also associated with powdery mildew resistance in Suwon 92, and explained 43 to 51% of the phenotypic variance. The powdery mildew resistance gene in Suwon 92 was located on the short arm of chromosome 1A where Pm3 was located. Two gene-specific markers were developed based on the sequence of the cloned Pm3b gene. These two markers, which were mapped at the same locus in the peak region of the LOD score for the RIL population, explained most of the phenotypic variance for powdery mildew resistance in the RIL population. The powdery mildew resistance in Suwon 92 is most likely conditioned by the Pm3 locus. The gene markers developed herein can be directly used for MAS of some of the Pm3 alleles in breeding programs.

Virulence of Oat Crown Rust in Mexico.

Virulence of isolates of Puccinia coronata collected during 1992 to 1998 from Sonora, Chihua-hua, Nuevo Leon, and five states in Central Mexico were compared on a set of 27 differential oat (Avena sativa) lines with different genes for race-specific resistance. Frequencies of virulence and the presence of specific pathogenic races were compared among the four regions of Mexico and between Mexico and the adjoining states of California and Texas in the United States. The P. coronata populations in Mexico were highly diverse even though the sexual stage of the fungus is not known to occur there. Overall virulence frequencies were most similar between Chihuahua and Nuevo Leon, but there were more races in common between Central Mexico and Chihuahua than between any other pair of regions of Mexico. No races found in Sonora were found in other regions of Mexico. More races found in Texas also occurred in Nuevo Leon than in any other region of Mexico. Mean virulence complexity was lowest in isolates from central Mexico; greatest in Sonora, California, and Texas; and intermediate in Chihuahua and Nuevo Leon. Significant (P < 0.05) associations of virulences occurred for 24 pairs of virulence genes in at least three of the four regions of Mexico. Virulences to 19 of the 24 pairs were also significantly associated in Texas; virulences to 13 were also significantly associated in California.

RAR1 Positively Controls Steady State Levels of Barley MLA Resistance Proteins and Enables Sufficient MLA6 Accumulation for Effective Resistance

The polymorphic barley (Hordeum vulgare) Mla locus harbors allelic race-specific resistance (R) genes to the powdery mildew fungus Blumeria graminis f sp hordei. The highly sequence-related MLA proteins contain an N-terminal coiled-coil structure, a central nucleotide binding (NB) site, a Leu-rich repeat (LRR) region, and a C-terminal non-LRR region. Using transgenic barley lines expressing epitope-tagged MLA1 and MLA6 derivatives driven by native regulatory sequences, we show a reversible and salt concentration-dependent distribution of the intracellular MLA proteins in soluble and membrane-associated pools. A posttranscriptional process directs fourfold greater accumulation of MLA1 over MLA6. Unexpectedly, in rar1 mutant plants that are compromised for MLA6 but not MLA1 resistance, the steady state level of both MLA isoforms is reduced. Furthermore, differential steady state levels of MLA1/MLA6 hybrid proteins correlate with their requirement for RAR1; the RAR1-independent hybrid protein accumulates to higher levels and the RAR1-dependent one to lower levels. Interestingly, yeast two-hybrid studies reveal that the LRR domains of RAR1-independent but not RAR1-dependent MLA isoforms interact with SGT1, a RAR1 interacting protein required for the function of many NB-LRR type R proteins. Our findings implicate the existence of a conserved mechanism to reach minimal NB-LRR R protein thresholds that are needed to trigger effective resistance responses.

Identification and transcriptional analysis of powdery mildew-induced barley genes

Differential screening by subtractive hybridisation and a random primer approach revealed 19 barley cDNAs representing gene transcripts, which accumulate during attack of Blumeria graminis f.sp. hordei race A6 ( BghA6) in barley lines carrying the race specific resistance gene Mlg. The encoded proteins were in part not reported from plant-pathogen interactions, so far, such as a putative blue copper binding protein and a putative tyrosine phosphatase. To elucidate a potential link between different types of powdery mildew resistance, we compared gene expression profiles in the interaction of barley with the appropriate BghA6, the inappropriate wheat powdery mildew fungus ( Bgt), and upon chemical treatment with the resistance-inducing chemical benzothiadiazole (BTH). Except for a tyrosine phosphatase gene, all the genes were induced after inoculation with the nonhost pathogen Bgt, and 18 genes were induced by appropriate BghA6 in plants lacking the race-specific Mlg gene while only three genes were stronger expressed after treatment with BTH. The copper binding protein and CJP74, a gene without known homologs, showed a higher BghA6-induced expression in resistant Mlg-lines compared to susceptible near-isogenic ( mlg) lines. Together, these findings suggest a significant overlap between basal, race-specific and nonhost resistance.

Late blight resistance in a diploid full‐sib potato family

AbstractLate blight, caused by Phytophthora infestans (Mont.) de Bary, is the most destructive disease of potato worldwide. As this pathogen can rapidly overcome major race‐specific resistance genes, identifying the basis for enhanced quantitative resistance has become a crucial element for implementing advanced breeding strategies. A population of 230 full‐sib progeny derived from a cross between two diploid hybrid Solanum phureja × S. stenotomum clones was evaluated for foliage resistance against late blight in replicated trials at multiple locations in Pennsylvania between 1999 and 2002. In field experiments, plants were evaluated visually for per cent defoliation, and area under the disease progress curve (AUDPC) was determined. The two parents and three control cultivars (‘Atlantic’, ‘Kennebec’ and ‘Katahdin’) were included in all trials. In all three experiments, the presence of a significant number of clones exhibiting transgressive segregation were observed. There were significant differences among environments as well as among clones, and the clone × environment interaction was also significant. Stability analysis revealed that 37 clones made a significant contribution to the overall environment × clone interaction. Broad‐sense heritability for resistance, measured as AUDPC, was estimated as 0.67. The overall results indicate the presence in this potato family of a high level of field resistance against late blight. This segregating diploid family appears to be a good candidate for quantitative trait loci mapping to identify and characterize the genetic components of partial late blight resistance.

A Computer Program to Improve the Efficiency and Accuracy of Postulating Race-Specific Resistance Genes.

Gene postulation has been the most widely used technique to determine the presence of particular rust resistance genes in lines of small grains. It applies the principles of gene-for-gene specificity to determine the most probable race-specific resistance genes present in host lines. As the numbers of lines, resistance genes, and races increase, postulation based on visual comparisons of infection types becomes more complex and laborious, and errors may occur. A computer program was developed to facilitate identification of race-specific leaf rust (Lr) genes in wheat (Triticum aestivum). Seedlings of 116 contemporary lines of soft red winter wheat and 24 Thatcher isolines (each Thatcher isoline with a single Lr gene) were inoculated with 22 races of Puccinia triticina. Infection types were recorded on the standard 0 to 4 scale where infection types 3 and 4 were considered high (line was susceptible; race was virulent) and others were low (line was resistant; race was avirulent). Based on the gene-for-gene concept, lines susceptible to a particular race cannot have an Lr gene for which the race is avirulent. For each line, step 1 of the program summarized results from races that were virulent on the line to definitively exclude Lr genes from the line, and this exclusion resulted in a relatively short list of Lr genes that could be present. Step 2 of the program utilized data from races that were avirulent on the line, and the output listed the low infection types produced on the line and the isolines with Lr genes that were not excluded in step 1. Of these Lr genes, a gene was considered present if the low infection type produced on the line by one or more races matched the low infection type on the corresponding isoline. Otherwise, the gene was considered possibly present. Epistatic effects of one or more Lr genes prevented definitive inclusion or exclusion of genes considered possibly present. If the low infection type produced on the line was lower than that on any of the isolines listed in step 2, then the line was considered to have an unidentified Lr gene; i.e., a gene that was not in the set of 24 isolines. This program facilitated the objective and accurate postulation of Lr genes and could be adapted to other host-pathogen systems.

SNARE-protein-mediated disease resistance at the plant cell wall.

Failure of pathogenic fungi to breach the plant cell wall constitutes a major component of immunity of non-host plant species--species outside the pathogen host range--and accounts for a proportion of aborted infection attempts on 'susceptible' host plants (basal resistance). Neither form of penetration resistance is understood at the molecular level. We developed a screen for penetration (pen) mutants of Arabidopsis, which are disabled in non-host penetration resistance against barley powdery mildew, Blumeria graminis f. sp. hordei, and we isolated the PEN1 gene. We also isolated barley ROR2 (ref. 2), which is required for basal penetration resistance against B. g. hordei. The genes encode functionally homologous syntaxins, demonstrating a mechanistic link between non-host resistance and basal penetration resistance in monocotyledons and dicotyledons. We show that resistance in barley requires a SNAP-25 (synaptosome-associated protein, molecular mass 25 kDa) homologue capable of forming a binary SNAP receptor (SNARE) complex with ROR2. Genetic control of vesicle behaviour at penetration sites, and plasma membrane location of PEN1/ROR2, is consistent with a proposed involvement of SNARE-complex-mediated exocytosis and/or homotypic vesicle fusion events in resistance. Functions associated with SNARE-dependent penetration resistance are dispensable for immunity mediated by race-specific resistance (R) genes, highlighting fundamental differences between these two resistance forms.

ESTABLISHMENT OF BIOTROPHY BY PARASITIC FUNGI AND REPROGRAMMING OF HOST CELLS FOR DISEASE RESISTANCE

Parasitic biotrophs such as mildews and rusts evolved specific mechanisms that keep host cells alive during infection. These fungi appear to absorb nutrients mainly by proton-symport-driven transporter proteins that reside in specialized feeding structures. Accumulating evidence suggests that biotrophic fungi both suppress induction of plant defense responses in physical proximity to infection sites and induce specific host genes for the establishment of biotrophy. The peculiarities of biotrophic pathogenesis likely reflect diverse types of plant disease-resistance responses. The cloning of race-specific resistance genes to powdery mildew infection and of genes required for their function provides first insights into molecular mechanisms enabling the host to recognize mildew effector components and suggests candidate mechanisms of resistance signaling. Resistance to powdery mildew fungi that result from mutations in host genes promises to shed light on mechanisms that are required for the establishment of disease susceptibility.

Chromosomal location of a race-specific resistance gene to Mycosphaerella graminicola in the spring wheat ST6.

Septoria tritici blotch, caused by Mycosphaerella graminicola, is a serious foliar disease of wheat worldwide. Qualitative, race-specific resistance sources have been identified and utilized for resistant cultivar development. However, septoria tritici blotch resistant varieties have succumbed to changes in virulence of M. graminicola on at least three continents. The use of resistance gene pyramids may slow or prevent the breakdown of resistance. A clear understanding of the genetics of resistance and the identification of linked PCR-based markers will facilitate the recovery of wheat lines carrying multiple septoria tritici blotch resistance genes. The resistance gene in ST6 to isolate MG2 of M. graminicola was mapped with microsatellite markers in two populations, ST6/Erik and ST6/Katepwa. Bulk segregant analysis identified a marker on chromosome 4AL putatively linked to the resistance gene. A large linkage group was identified in each population using additional microsatellite markers mapping to chromosome 4AL. The resistance gene in ST6 mapped to the distal end of chromosome 4AL in each mapping population and was designated Stb7. Three of the microsatellite loci, Xwmc313, Xwmc219 and Xgwm160, mapped within 3.5 cM of Stb7; however, none flanked Stb7. Xwmc313 was the closest and mapped 0.3 and 0.5 cM from Stb7 in the crosses ST6/Katepwa and ST6/Erik, respectively. WMC313 will be very useful for marker-assisted selection of Stb7 in Canadian breeding programs because the ST6 allele of Xwmc313 was not identified in any of the Canadian common wheat cultivars tested.

Differential responses to pea bacterial blight in stems, leaves and pods under glasshouse and field conditions

Resistance to pea bacterial blight (Pseudomonas syringae pv. pisi) in different plant parts was assessed in 19 Pisum sativum cultivars and landraces, carrying race-specific resistance genes (R-genes) and two Pisum abyssinicum accessions carrying race-nonspecific resistance. Stems, leaves and pods were inoculated with seven races of P. s. pv. pisi under glasshouse conditions. For both race-specific and nonspecific resistance, a resistant response in the stem was not always associated with resistance in leaf and pod. Race-specific genes conferred stem resistance consistently, however, there was variability in the responses of leaves and pods which depended on the matching R-gene and A-gene (avirulence gene in the pathogen) combination. R2 generally conferred resistance in all plant parts. R3 or R4 singly did not confer complete resistance in leaf and pod, however, R3 in combination with R2 or R4 enhanced leaf and pod resistance. Race-nonspecific resistance conferred stem resistance to all races, leaf and pod resistance to races 2, 5 and 7 and variable reactions in leaves and pods to races 1, 3, 4 and 6. Disease expression was also studied in the field under autumn/winter conditions. P. sativum cultivar, Kelvedon Wonder (with no R genes), and two P. abyssinicum accessions, were inoculated with the most frequent races in Europe under field conditions (2, 4 and 6). Kelvedon Wonder was very susceptible to all three races, whereas P. abyssinicum was much less affected. The combination of disease resistance with frost tolerance in P. abyssinicum enabled plants to survive through the winter. A breeding strategy combining race-nonspecific resistance derived from P. abyssinicum with race-specific R-genes should provide durable resistance under severe disease pressure.

Screening and identification of resistance to Leptosphaeria maculans (stem canker) in Brassica napus accessions

The occurrence of race-specific resistance genes to the stem canker fungus, Leptosphaeria maculans, was analysed in 453 accessions of B. napus, mainly originating from the Institut fur Pflanzengenetik und Kulturpflanzenforschung (IPK) GeneBank. Major resistance genes Rlm1, Rlm2, Rlm4 and the putative RlmBBA gene were investigated using genetically improved strains of the fungus harbouring as few corresponding avirulence genes as possible. In addition, a screening with fully virulent isolates was used to uncover novel resistance sources. Major resistance genes were rarer in frequency and diversity in spring-type cultivars compared to winter types. In the former, 65.7% of the accessions were fully susceptible to all isolates, whereas only 12.2% of the winter types were devoid of at least one R gene. In spring cultivars, the most common R gene, Rlm4 was found in 26.6% of accessions, whereas the other R genes were rare. In winter cultivars, the most common R genes were Rlm2 (more than 45.9–54.0% of the accessions) and Rlm4 (26.4–27.7% of the genotypes). In winter types however, the improvement of the quality of oils, through the generation of single- and double-low genotypes improved the homogeneity of the cvs, whereas it impoverished R gene diversity, including the loss of complete resistance that was harboured by 18.4% of the less advanced accessions, and a reduction in the ratio of accessions harbouring Rlm1. Correlation between the R gene(s) present in the accessions and their field resistance is discussed.