Identification of quantitative trait loci for resistance to <Emphasis Type="Italic">Xanthomonas campestris</Emphasis> pv. <Emphasis Type="Italic">campestris</Emphasis> in <Emphasis Type="Italic">Brassica rapa</Emphasis>

Resistance to six known races of black rot in crucifers caused by Xanthomonas campestris pv. campestris (Pammel) Dowson is absent or very rare in Brassica oleracea (C genome). However, race specific and broad-spectrum resistance (to type strains of all six races) does appear to occur frequently in other brassica genomes including B. rapa (A genome). Here, we report the genetics of broad spectrum resistance in the B. rapa Chinese cabbage accession B162, using QTL analysis of resistance to races 1 and 4 of the pathogen. A B. rapa linkage map comprising ten linkage groups (A01–A10) with a total map distance of 664 cM was produced, based on 223 AFLP bands and 23 microsatellites from a F₂ population of 114 plants derived from a cross between the B. rapa susceptible inbred line R-o-18 and B162. Interaction phenotypes of 125 F₂ plants were assessed using two criteria: the percentage of inoculation sites in which symptoms developed, and the severity of symptoms per plant. Resistance to both races was correlated and a cluster of highly significant QTL that explained 24–64% of the phenotypic variance was located on A06. Two additional QTLs for resistance to race 4 were found on A02 and A09. Markers closely linked to these QTL could assist in the transference of the resistance into different B. rapa cultivars or into B. oleracea.     

Identification of QTL for resistance and susceptibility to <Emphasis Type="Italic">Stagonospora meliloti</Emphasis> in autotetraploid lucerne

In eastern Australia and California, USA, one of the major lethal fungal diseases of lucerne (Medicago sativa) is Stagonospora root and crown rot, caused by Stagonospora meliloti. Quantitative trait loci (QTL) involved in resistance and susceptibility to S. meliloti were identified in an autotetraploid lucerne backcross population of 145 individuals. Using regression analysis and interval mapping, we detected one region each on linkage groups 2, 6 and 7 that were consistently associated with disease reaction to S. meliloti in two separate experiments. The largest QTL on linkage group 7, which is associated with resistance to S. meliloti, contributed up to 17% of the phenotypic variation. The QTL located on linkage group 2, which is potentially a resistance allele in repulsion to the markers for susceptibility to S. meliloti, contributed up to 8% of the phenotypic variation. The QTL located on linkage group 6, which is associated with susceptibility to S. meliloti, contributed up to 16% of the phenotypic variation. A further two unlinked markers contributed 5 and 8% of the phenotypic variation, and were detected in only one experiment. A total of 517 simple sequence repeat (SSR) markers from Medicago truncatula were screened on the parents of the mapping population. Only 27 (6%) SSR markers were polymorphic and could be incorporated into the autotetraploid map of M. sativa. This allowed alignment of our M. sativa linkage map with published M. truncatula maps. The markers linked to the QTL we have reported will be useful for marker assisted selection for partial resistance to S. meliloti in lucerne.     

Identification of novel genomic regions associated with resistance to <Emphasis Type="Italic">Pyrenophora tritici</Emphasis>-<Emphasis Type="Italic">repentis</Emphasis> races 1 and 5 in spring wheat landraces using association analysis

Tan spot, caused by Pyrenophora tritici-repentis, is a major foliar disease of wheat worldwide. Host plant resistance is the best strategy to manage this disease. Traditionally, bi-parental mapping populations have been used to identify and map quantitative trait loci (QTL) affecting tan spot resistance in wheat. The association mapping (AM) could be an alternative approach to identify QTL based on linkage disequilibrium (LD) within a diverse germplasm set. In this study, we assessed resistance to P. tritici-repentis races 1 and 5 in 567 spring wheat landraces from the USDA-ARS National Small Grains Collection (NSGC). Using 832 diversity array technology (DArT) markers, QTL for resistance to P. tritici-repentis races 1 and 5 were identified. A linear model with principal components suggests that at least seven and three DArT markers were significantly associated with resistance to P. tritici-repentis races 1 and 5, respectively. The DArT markers associated with resistance to race 1 were detected on chromosomes 1D, 2A, 2B, 2D, 4A, 5B, and 7D and explained 1.3–3.1% of the phenotypic variance, while markers associated with resistance to race 5 were distributed on 2D, 6A and 7D, and explained 2.2–5.9% of the phenotypic variance. Some of the genomic regions identified in this study correspond to previously identified loci responsible for resistance to P. tritici-repentis, offering validation for our AM approach. Other regions identified were novel and could possess genes useful for resistance breeding. Some DArT markers associated with resistance to race 1 also were localized in the same regions of wheat chromosomes where QTL for resistance to yellow rust, leaf rust and powdery mildew, have been mapped previously. This study demonstrates that AM can be a useful approach to identify and map novel genomic regions involved in resistance to P. tritici-repentis.     

Molecular mapping of resistance to <Emphasis Type="Italic">Pyrenophora tritici-repentis</Emphasis> race 5 and sensitivity to Ptr ToxB in wheat

Tan spot, caused by Pyrenophora tritici-repentis (Ptr), is an economically important foliar disease in the major wheat growing areas of the world. Multiple races of the pathogen have been characterized based on their ability to cause necrosis and/or chlorosis in differential wheat lines. Isolates of race 5 cause chlorosis only, and they produce a host-selective toxin designated Ptr ToxB that induces chlorosis when infiltrated into sensitive genotypes. The international Triticeae mapping initiative (ITMI) mapping population was used to identify genomic regions harboring QTLs for resistance to fungal inoculations of Ptr race 5 and to determine the chromosomal location of the gene conditioning sensitivity to Ptr ToxB. The toxin-insensitivity gene, which we are designating tsc2, mapped to the distal tip of the short arm of chromosome 2B. This gene was responsible for the effects of a major QTL associated with resistance to the race 5 fungus and accounted for 69% of the phenotypic variation. Additional minor QTLs were identified on the short arm of 2A, the long arm of 4A, and on the long arm of chromosome 2B. Together, the major QTL on 2BS identified by tsc2 and the QTL on 4AL explained 73% of the total phenotypic variation for resistance to Ptr race 5. The results of this research indicate that Ptr ToxB is a major virulence factor, and the markers closely linked to tsc2 and the 4A QTL should be useful for introgression of resistance into adapted germplasm.     

Linkage mapping of genes controlling resistance to white rust (Albugo candida) in Brassica rapa (syn. campestris) and comparative mapping to Brassica napus and Arabidopsis thaliana.

Genes for resistance to white rust (Albugo candida) in oilseed Brassica rapa were mapped using a recombinant inbred (RI) population and a genetic linkage map consisting of 144 restriction fragment length polymorphism (RFLP) markers and 3 phenotypic markers. Young seedlings were evaluated by inoculating cotyledons with A. candida race 2 (AC2) and race 7 (AC7) and scoring the interaction phenotype (IP) on a 0-9 scale. The IP of each line was nearly identical for the two races and the population showed bimodal distributions, suggesting that a single major gene (or tightly linked genes) controlled resistance to the two races. The IP scores were converted to categorical resistant and susceptible scores, and these data were used to map a single Mendelian gene controlling resistance to both races on linkage group 4 where resistance to race 2 had been mapped previously. A quantitative trait loci (QTL) mapping approach using the IP scores detected the same major resistance locus for both races, plus a second minor QTL effect for AC2 on linkage group 2. These results indicate that either a dominant allele at a single locus (Acal) or two tightly linked loci control seedling resistance to both races of white rust in the biennial turnip rape cultivar Per. The map positions of white rust resistance genes in B. rapa and Brassica napus were compared and the results indicate where additional loci that have not been mapped may be located. Alignment of these maps to the physical map of the Arabidopsis genome identified regions to target for comparative fine mapping using this model organism.     

Molecular characterisation of resistance against potato wart races 1, 2, 6 and 18 in a tetraploid population of potato (Solanum tuberosum subsp. tuberosum)

Potato wart is caused by the obligate biotrophic fungus Synchytrium endobioticum, which is subject to quarantine regulations due to the production of long persisting spores in the soil and the lack of effective fungicides. The objective of this study was to identify quantitative trait loci (QTL) for resistance against potato wart races (R) 1, 2, 6 and 18 in a tetraploid potato population developed by crossing cv. Saturna (resistant to R1) with cv. Panda (resistant to R1, R2, R6, R18). A total of 92 progenies were used for phenotyping and genotyping. Resistance tests were performed for races 1 and 18 in 2 years and for races 2 and 6 in 1 year on 10 to 20 eyepieces per genotype. Based on amplified fragment length polymorphism (AFLP) and simple sequence repeat (SSR) markers, linkage maps were established for the female and male parent, respectively. Single marker analysis followed by a multiple regression analysis revealed initial marker–trait associations. The interval mapping routine of TetraploidMap was applied for QTL analysis. A major QTL for resistance against race 1 explaining between 46 % and 56 % of the phenotypic variation was identified near Sen1, a known resistance locus for potato wart race 1 on chromosome XI. Other resistance QTL were detected on chromosomes I (to R2), II (to R6, 18), VI (to R1, 2, 6, 18), VII (to R2, 6, 18), VIII (to R1, 2, 6, 18), X (to R2, 6, 18), XI (to R2, 6, 18) and on an unknown linkage group (to R18) explaining minor to moderate effects of the phenotypic variation. Resistance QTL against different potato wart races often overlapped, particularly concerning races 2, 6 and 18. Overall, this study gives a valuable insight into the complex inheritance of resistance against potato wart.     

Identification and molecular mapping of PdR1, a primary resistance gene to Pierce’s disease in Vitis

A major quantitative trait locus (QTL) controlling resistance to Pierce’s disease (PD) of grape, caused by the bacterium Xylella fastidiosa (Xf), was identified on a Vitis linkage map and denoted as ‘Pierce’s disease resistance 1’ (PdR1). Placement of the locus was accomplished by evaluating a family of full-sib progeny from a cross of two PD-resistant interspecific hybrids with resistance inherited from Vitis arizonica. Resistance was measured under greenhouse conditions by direct quantification of Xf numbers in stem tissues as well as by evaluation of disease symptoms based on leaf scorch and a cane maturation index (CMI). A large QTL (LOD 17.2) accounting for 72% of the phenotypic variance in bacterial numbers was localized to linkage group 14 of the male parent F8909-17. The approximate 95% confidence interval around the QTL peak extended 5.7 cM when using composite interval mapping. The other disease evaluation methods (leaf scorch and CMI, respectively) placed the resistance QTL to the same region on linkage group 14, although at wider 95% confidence intervals (6.0 and 7.5 cM), lower peak LOD scores (11.9 and 7.7) and accounting for less phenotypic variance (59 and 42%). This is the first report of an Xf resistance QTL mapped in any crop species. The relevance of the markers located in the region spanning the QTL will be discussed, addressing their usefulness for the development of PD-resistant grape cultivars.     

Codominant PCR-based markers and candidate genes for powdery mildew resistance in melon (<Emphasis Type="Italic">Cucumis melo</Emphasis> L.)

Powdery mildew caused by Podosphaera xanthii is a major disease in melon crops, and races 1, 2, and 5 of this fungus are those that occur most frequently in southern Europe. The genotype TGR-1551 bears a dominant gene that provides resistance to these three races of P. xanthii. By combining bulked segregant analysis and amplified fragment length polymorphisms (AFLP), we identified eight markers linked to this dominant gene. Cloning and sequencing of the selected AFLP fragments allowed the development of six codominant PCR-based markers which mapped on the linkage group (LG) V. Sequence analysis of these markers led to the identification of two resistance-like genes, MRGH5 and MRGH63, belonging to the nucleotide binding site (NBS)-leucine-rich repeat (LRR) gene family. Quantitative trait loci (QTL) analysis detected two QTLs, Pm-R1-2 and Pm-R5, the former significantly associated with the resistance to races 1 and 2 (LOD score of 26.5 and 33.3; 53.6 and 61.9% of phenotypic variation, respectively), and the latter with resistance to race 5 (LOD score of 36.8; 65.5% of phenotypic variation), which have been found to be colocalized with the MRGH5 and MRGH63 genes, respectively. The results suggest that the cluster of NBS-LRR genes identified in LG V harbours candidate genes for resistance to races 1, 2, and 5 of P. xanthii. The evaluation of other resistant germplasm showed that the codominant markers here reported are also linked to the Pm-w resistance gene carried by the accession ‘WMR-29’ proving their usefulness as genotyping tools in melon breeding programmes.     

Loss of resistance to Colletotrichum trifolii in in vitro regenerated alfalfa

Alfalfa plants were regenerated from callus cultures of three source plants that differed in resistance to anthracnose, caused by Colletotrichum trifolii. All regenerant plants were evaluated for variation in resistance to disease caused by races 1 and 2 of the pathogen. Of eighty-two plants that were regenerated and evaluated, no plants responded differently to inoculation with race 1 of C. trifolii, but two plants (2.4%) differed in resistance when inoculated with race 2. The source plant of these regenerants was resistant to races 1 and 2 of the pathogen but the regenerants were resistant to race 1 and susceptible to race 2. No variants to race 1 were detected. The susceptible response of the variant plants to race 2 was confirmed by cytological analysis and was consistent with the response of nonregenerant susceptible plants. These plants represent a near-isogenic plant model for studying the molecular biology of resistance and susceptibility to anthracnose of alfalfa.     

Genetic linkage map of melon (<Emphasis Type="Italic">Cucumis melo</Emphasis> L.) and localization of a major QTL for powdery mildew resistance

Powdery mildew caused by Podosphaera xanthii has become a major problem in melon since it occurs all year round irrespective of the growing system. The TGR-1551 melon genotype was found to be resistant to several melon diseases, among them powdery mildew. However, the corresponding resistance genes have been never mapped. We constructed an integrated genetic linkage map using an F2 population derived from a cross between the multi-resistant genotype TGR-1551 and the susceptible Spanish cultivar ‘Bola de Oro’. The map spans 1,284.9 cM, with an average distance of 3.6 cM among markers, and consists of 354 loci (188 AFLP, 39 RAPD, 111 SSR, 14 SCAR/CAPS/dCAPS, and two phenotypic traits) distributed in 14 linkage groups. QTL analysis identified one major QTL (Pm-R) on LG V for resistance to races 1, 2, and 5 of powdery mildew. The PM4-CAPS marker is closely linked to the Pm-R QTL at a genetic distance of 1.9 cM, and the PM3-CAPS marker is located within the support interval of this QTL. These codominant markers, together with the map information reported here, could be used for melon breeding, and particularly for genotyping selection of resistance to powdery mildew in this vegetable crop species.     

An anchored linkage map for sugar beet based on AFLP,SNP and RAPD markers and QTL mapping of a new source of resistance to <Emphasis Type="Italic">Beet necrotic yellow vein virus</Emphasis>

Rhizomania, caused by Beet necrotic yellow vein virus (BNYVV), is an important sugar-beet disease worldwide and can result in severe losses of root yield and sugar content. We have identified a major QTL for BNYVV resistance from a new source in a segregating population of 158 individuals. The QTL explained an estimated 78% of the observed phenotypic variation and the gene conferring the partial resistance is referred to as Rz4. AFLP was used in combination with bulked segregant analysis (BSA) to develop markers linked to the resistance phenotype. AFLP marker analysis was extended to produce a linkage map that was resolved into nine linkage groups. These were anchored to the nine sugar-beet chromosomes using previously published SNP markers. This represents the first anchored sugar-beet linkage map to be published with non-anonymous markers. The final linkage map comprised 233 markers covering 497.2 cM, with an average interval between markers of 2.1 cM. The Rz4 QTL and an Rz1 RAPD marker were mapped to chromosome III, the known location of the previously identified BNYVV resistance genes Rz1, Rz2 and Rz3. The availability to breeders of new resistance sources such as Rz4 increases the potential for breeding durable disease resistance.     

Construction of a linkage map based on a <Emphasis Type="Italic">Lathyrus sativus</Emphasis> backcross population and preliminary investigation of QTLs associated with resistance to ascochyta blight

A linkage map of the Lathyrus sativus genome was constructed using 92 backcross individuals derived from a cross between an accession resistant (ATC 80878) to ascochyta blight caused by Mycosphaerella pinodes and a susceptible accession (ATC 80407). A total of 64 markers were mapped on the backcross population, including 47 RAPD, seven sequence-tagged microsatellite site and 13 STS/CAPS markers. The map comprised nine linkage groups, covered a map distance of 803.1 cM, and the average spacing between markers was 15.8 cM. Quantitative trait loci (QTL) associated with ascochyta blight resistance were detected using single-point analysis and simple and composite interval mapping. The backcross population was evaluated for stem resistance in temperature-controlled growth room trials. One significant QTL, QTL1, was located on linkage group 1 and explained 12% of the phenotypic variation in the backcross population. A second suggestive QTL, QTL2, was detected on linkage group 2 and accounted for 9% of the trait variation. The L. sativus R-QTL regions detected may be targeted for future intergenus transfer of the trait into accessions of the closely related species Pisum sativum.     

Molecular mapping of a new source of Fusarium wilt resistance in tetraploid cotton (Gossypium hirsutum L.)

Fusarium wilt (FW) disease is an economically important disease of cotton worldwide and a major cause of crop losses in Australia and many other cotton-producing countries. Symptoms include wilting, vascular browning and death. Australian races of the causal agent Fusarium oxysporum f. sp. vasinfectum (Fov) are genetically distinct from those in other countries and are thought to have evolved from indigenous races. New sources of resistance for breeding are rare, as cotton cultivars with significant FW resistance against Fov isolates from other cotton-producing regions are usually susceptible to Australian Fov races. MCU-5, an Upland Indian cotton cultivar, has been identified as having improved resistance to Australian Fov and is being used to breed new commercial cultivars with higher resistance to FW. To investigate the genetic basis of the FW resistance in MCU-5, QTL analysis was performed on 244 F3 and 244 F4 families derived from an intraspecific cross between MCU-5 and Siokra 1-4, a cultivar highly sensitive to Australian Fov races. Resistance, as measured by leaf symptoms, vascular browning and survival, showed low to moderate heritability between generations. MCU-5 resistance to FW was found to be complex with three quantitative trait loci (QTL) identified in the F3, and eight in the F4, that explained between 9 and 41% of the phenotypic variation. The QTL were located on four linkage groups including chromosomes A6 (Chr 6), D4 (Chr 22) and D6 (Chr 25), with two QTL located in similar regions to previously identified FW resistance from the Sea Island cultivar Pima 3-79. The QTL identified in this study represent the first targets for marker-assisted selection of FW resistance in Australia.     

Strain-specific and recessive QTLs involved in the control of partial resistance to Fusarium oxysporum f. sp. melonis race 1.2 in a recombinant inbred line population of melon

Fusarium oxysporum f. sp. melonis (FOM) causes serious economic losses in melon (Cucumis melo L.). Two dominant resistance genes have been identified, Fom-1 and Fom-2, which provide resistance to races 0 and 2 and races 0 and 1, respectively, however FOM race 1.2 overcomes these resistance genes. A partial resistance to FOM race 1.2 that has been found in some Far East accessions is under polygenic control. A genetic map of melon was constructed to tag FOM race 1.2 resistance with DNA markers on a recombinant inbred line population derived from a cross between resistant (Isabelle) and susceptible (cv. Védrantais) lines. Artificial root inoculations on plantlets of this population using two strains, one that causes wilting (FOM 1.2w) and one that causes yellowing (FOM 1.2y), resulted in phenotypic and genotypic data that enabled the identification of nine quantitative trait loci (QTLs). These QTLs were detected on five linkage groups by composite interval mapping and explained between 41.9% and 66.4% of the total variation. Four digenic epistatic interactions involving seven loci were detected and increased the total phenotypic variation that was explained. Co-localizations between QTLs and resistance gene homologs or resistance genes, such as Fom-2 and Vat, were observed. A strain-specific QTL was detected, and some QTLs appeared to be recessive.     

A genetic linkage map of <Emphasis Type="Italic">Phaseolus vulgaris</Emphasis> L. and localization of genes for specific resistance to six races of anthracnose (<Emphasis Type="Italic">Colletotrichum lindemuthianum</Emphasis>)

A genetic map of common bean was constructed using 197 markers including 152 RAPDs, 32 RFLPs, 12 SCARs, and 1 morphological marker. The map was established by using a F₂ population of 85 individuals from the cross between a line derived from the Spanish landrace Andecha (Andean origin) and the Mesoamerican genotype A252. The resulting map covers about 1,401.9 cM, with an average marker distance of 7.1 cM and includes molecular markers linked to disease resistance genes for anthracnose, bean common mosaic virus, bean golden yellow mosaic virus, common bacterial blight, and rust. Resistance to races 6, 31, 38, 39, 65, and 357 of the pathogenic fungus Colletotrichum lindemuthianum (anthracnose) was evaluated in F₃ families derived from the corresponding F₂ individuals. The intermediate resistance to race 65 proceeding from Andecha can be explained by a single dominant gene located on linkage group B1, corresponding to the Co-1 gene. The recombination between the resistance specificities proceeding from A252 agrees with the assumption that total resistance to races 6, 31, 38, 39, 65, and 357, is organized in two clusters. One cluster, located on B4 linkage group, includes individual genes for specific resistance to races 6, 38, 39, and 357. The second cluster is located on linkage group B11 and includes individual genes for specific resistance to races 6, 31, 38, 39, and 65. These two clusters correspond to genes Co-3/Co-9 and Co-2, respectively. It is concluded that most anthracnose resistance Co- genes, previously described as single major genes conferring resistance to several races, could be organized as clusters of different genes conferring race-specific resistance. C. Rodríguez-Suárez and B. Méndez-Vigo equally share for authorship.     

Anther extrusion and plant height are associated with Type I resistance to Fusarium head blight in bread wheat line ‘Shanghai-3/Catbird’

Fusarium head blight (FHB) is a destructive wheat disease of global importance. Resistance breeding depends heavily on the Fhb1 gene. The CIMMYT line Shanghai-3/Catbird (SHA3/CBRD) is a promising source without this gene. A recombinant inbred line (RIL) population from the cross of SHA3/CBRD with the German spring wheat cv. Naxos was evaluated for FHB resistance and related traits in field trials using spray and spawn inoculation in Norway and point inoculation in China. After spray and spawn inoculation, FHB severities were negatively correlated with both anther extrusion (AE) and plant height (PH). The QTL analysis showed that the Rht-B1b dwarfing allele co-localized with a QTL for low AE and increased susceptibility after spawn and spray inoculation. In general, SHA3/CBRD contributed most of the favorable alleles for resistance to severity after spray and spawn inoculation, while Naxos contributed more favorable alleles for reduction in FDK and DON content and resistance to severity after point inoculation. SHA3/CBRD contributed a major resistance QTL close to the centromere on 2DLc affecting FHB severity and DON after all inoculation methods. This QTL was also associated with AE and PH, with high AE and tall alleles contributed by SHA3/CBRD. Several QTL for AE and PH were detected, and low AE or reduced PH was always associated with increased susceptibility after spawn and spray inoculation. Most of the other minor FHB resistance QTL from SHA3/CBRD were associated with AE or PH, while the QTL from Naxos were mostly not. After point inoculation, no other QTL for FHB traits was associated with AE or PH, except the 2DLc QTL which was common across all inoculation methods. Marker-assisted selection based on the 2DLc QTL from SHA3/CBRD combined with phenotypic selection for AE is recommended for resistance breeding based on this valuable source of resistance.     

Genetic dissection of the resistance to nine anthracnose races in the common bean differential cultivars MDRK and TU

Resistance to nine races of the pathogenic fungus Colletotrichum lindemuthianum, causal agent of anthracnose, was evaluated in F₃ families derived from the cross between the anthracnose differential bean cultivars TU (resistant to races, 3, 6, 7, 31, 38, 39, 102, and 449) and MDRK (resistant to races, 449, and 1545). Molecular marker analyses were carried out in the F₂ individuals in order to map and characterize the anthracnose resistance genes or gene clusters present in these two differential cultivars. The results of the combined segregation indicate that at least three independent loci conferring resistance to anthracnose are present in TU. One of them, corresponding to the previously described anthracnose resistance locus Co-5, is located in linkage group B7, and is formed by a cluster of different genes conferring specific resistance to races, 3, 6, 7, 31, 38, 39, 102, and 449. Evidence of intra-cluster recombination between these specific resistance genes was found. The second locus present in TU confers specific resistance to races 31 and 102, and the third locus confers specific resistance to race 102, the location of these two loci remains unknown. The resistance to race 1545 present in MDRK is due to two independent dominant genes. The results of the combined segregation of two F₄ families showing monogenic segregation for resistance to race 1545 indicates that one of these two genes is linked to marker OF10₅₃₀, located in linkage group B1, and corresponds to the previously described anthracnose resistance locus Co-1. The second gene conferring resistance to race 1545 in MDRK is linked to marker Pv-ctt001, located in linkage group B4, and corresponds to the Co-3/Co-9 cluster. The resistance to race 449 present in MDRK is conferred by a single gene, located in linkage group B4, probably included in the same Co-3/Co-9 cluster. Electronic supplementary material  The online version of this article (doi:) contains supplementary material, which is available to authorized users.     

QTL influencing growth and wood properties in Eucalyptus globulus

Regions of the genome affecting physical and chemical wood properties (quantitative trait loci (QTL)), as well as growth, were identified using a clonally replicated, outbred F₂ family (112 genotypes, each with two ramets) of Eucalyptus globulus, planted in a field trial in north-west Tasmania. Traits studied were growth (assessed by stem diameter), wood density, cellulose content, pulp yield and lignin content. These traits are important in breeding for pulpwood, and will be important in breeding for carbon sequestration and biofuel production. Between one and four QTL were located for each trait, with each QTL explaining between 4% and 12% of the phenotypic variation. Several QTL for chemical wood properties were co-located, consistent with their high phenotypic correlations, and may reflect pleiotropic effects of the same genes. In contrast, QTL for density and lignin content with overlapping confidence intervals were considered to be due to independent genes, since the QTL effects were inherited from different parents. The inclusion of fully informative microsatellites on the linkage map allowed the determination of homology at the linkage group level between QTL and candidate genes in different pedigrees of E. globulus and different eucalypt species. None of the candidate genes mapped in comparable studies co-located with our major QTL for wood chemical properties, arguing that there are important candidate genes yet to be discovered.     

Identification of QTLs associated with resistance to soybean cyst nematode races 2, 3 and 5 in soybean PI 90763

Soybean cyst nematode (SCN) is a major soybean pest throughout the soybean growing regions in the world, including the USA. Soybean PI 90763 is an important SCN resistance source. It is resistant to several SCN populations including races 2, 3 and 5. But its genetics of resistance is not well known. The objectives of this study were to: (1) confirm quantitative trait loci (QTLs) for resistance to SCN race 3 in PI 90763 and (2) identify QTLs for resistance to SCN races 2 and 5. QTLs were searched in Hamilton × PI 90763 F_2:3populations using 193 polymorphic simple sequence repeats (SSRs) covering 20 linkage groups (LGs). QTLs for resistance to SCN were identified on LGs A2, B1, E, G, J and L. The same QTL was suggested for resistance to different SCN races where their 1-LOD support intervals of QTL positions highly overlapped. The QTL on LG G was associated with resistance to races 2, 3 and 5. The QTL on LG B1 was associated with resistance to races 2 and 5. The QTL on LG J was associated with resistance to races 2 and 3. The QTLs on LGs A2 and L were associated with resistance to race 3. The QTL on LG E was associated with resistance to race 5. We conclude that LGs A2 and B1 may represent an important distinction between resistance to SCN race 3 and resistance to SCN races 2 and 5 in soybean.     

Genetic dissection of tocopherol and phytosterol in recombinant inbred lines of sunflower through quantitative trait locus analysis and the candidate gene approach

Sunflower (Helianthus annuus L.) contains tocopherol, a non-enzymatic antioxidant known as lipid-soluble vitamin E, and phytosterol, with interesting properties, which can result in decreased risk of chronic diseases in humans and with several beneficial effects in plants. The genetic control of tocopherol and phytosterol content in a population of 123 recombinant inbred lines of sunflower was studied through quantitative trait loci (QTL) analysis using 190 simple sequence repeats and a gene-based linkage map. Seven experiments were conducted in different environments in France and Iran during 2007 and 2008. Each experiment consisted of three replications. Means over all environments were used for QTL mapping. Five QTL for total tocopherol content on linkage groups 1, 8, 10 and 14 accounted for 45% of phenotypic variation, whereas four QTL for total phytosterol content on linkage groups 1, 2, 16 and 17 explained 27% of the phenotypic variation. GST, PAT2, SFH3 and POD genes showed co-localization with QTL for total phytosterol content. SMT2 is also mapped on linkage group 17 near the QTL of total phytosterol content. Four candidate genes, VTE4, HPPD, GST and Droug1, exhibited co-localization with QTL for total tocopherol content. The candidate genes associated with tocopherol and phytosterol, especially HPPD, VTE4 and SMT2, could be used for alternation of the tocopherol and phytosterol content of sunflower seeds through the development of functional markers.