Integration of sudden death syndrome resistance loci in the soybean genome

Key message

Complexity and inconsistencies in resistance mapping publications of soybean sudden death syndrome (SDS) result in interpretation difficulty. This review integrates SDS mapping literature and proposes a new nomenclature system for reproducible SDS resistance loci.

Abstract

Soybean resistance to sudden death syndrome (SDS) is composed of foliar resistance to phytotoxins and root resistance to pathogen invasion. There are more than 80 quantitative trait loci (QTL) and dozens of single nucleotide polymorphisms (SNPs) associated with soybean resistance to SDS. The validity of these QTL and SNPs is questionable because of the complexity in phenotyping methodologies, the disease synergism between SDS and soybean cyst nematode (SCN), the variability from the interactions between soybean genotypes and environments, and the inconsistencies in the QTL nomenclature. This review organizes SDS mapping results and proposes the Rfv (resistance to Fusarium virguliforme) nomenclature based on supporting criteria described in the text. Among ten reproducible loci receiving our Rfv nomenclature, Rfv18-01 is mostly supported by field studies and it co-localizes to the SCN resistance locus rhg1. The possibility that Rfv18-01 is a pleiotropic resistance locus and the concern about Rfv18-01 being confounded with Rhg1 is discussed. On the other hand, Rfv06-01, Rfv06-02, Rfv09-01, Rfv13-01, and Rfv16-01 were identified both by screening soybean leaves against phytotoxic culture filtrates and by evaluating SDS severity in fields. Future phenotyping using leaf- and root-specific resistance screening methodologies may improve the precision of SDS resistance, and advanced genetic studies may further clarify the interactions among soybean genotypes, F. virguliforme, SCN, and environments. The review provides a summary of the SDS resistance literature and proposes a framework for communicating SDS resistance loci for future research considering molecular interactions and genetic breeding for soybean SDS resistance.

     

Field evaluation of three sources of genetic resistance to sudden death syndrome of soybean

Key message

Despite numerous challenges, field testing of three sources of genetic resistance to sudden death syndrome of soybean provides information to more effectively improve resistance to this disease in cultivars.

Abstract

Sudden death syndrome (SDS) of soybean [Glycine max (L.) Merrill] is a disease that causes yield loss in soybean growing regions across the USA and worldwide. While several quantitative trait loci (QTL) for SDS resistance have been mapped, studies to further evaluate these QTL are limited. The objective of our research was to map SDS resistance QTL and to test the effect of mapped resistance QTL on foliar symptoms when incorporated into elite soybean backgrounds. We mapped a QTL from Ripley to chromosome 10 (CHR10) and a QTL from PI507531 to chromosomes 1 and 18 (CHR1 and 18). Six populations were then developed to test the following QTL: cqSDS-001, with resistance originating from PI567374, CHR10, CHR1, and CHR18. The populations which segregated for resistant and susceptible QTL alleles were field tested in multiple environments and evaluated for SDS foliar symptoms. While foliar disease development was variable across environments and populations, a significant effect of each QTL on disease was detected within at least one environment. This includes the detection of cqSDS-001 in three genetic backgrounds. The QTL allele from the resistant parents was associated with greater resistance than the susceptible alleles for all QTL and backgrounds with the exception of the allele for CHR18, where the opposite occurred. This study highlights the importance and difficulties of evaluating QTL and the need for multi-year SDS field testing. The information presented in this study can aid breeders in making decisions to improve resistance to SDS.

     

SNP identification and marker assay development for high-throughput selection of soybean cyst nematode resistance

Background

Soybean cyst nematode (SCN) is the most economically devastating pathogen of soybean. Two resistance loci, Rhg1 and Rhg4 primarily contribute resistance to SCN race 3 in soybean. Peking and PI 88788 are the two major sources of SCN resistance with Peking requiring both Rhg1 and Rhg4 alleles and PI 88788 only the Rhg1 allele. Although simple sequence repeat (SSR) markers have been reported for both loci, they are linked markers and limited to be applied in breeding programs due to accuracy, throughput and cost of detection methods. The objectives of this study were to develop robust functional marker assays for high-throughput selection of SCN resistance and to differentiate the sources of resistance.

Results

Based on the genomic DNA sequences of 27 soybean lines with known SCN phenotypes, we have developed Kompetitive Allele Specific PCR (KASP) assays for two Single nucleotide polymorphisms (SNPs) from Glyma08g11490 for the selection of the Rhg4 resistance allele. Moreover, the genomic DNA of Glyma18g02590 at the Rhg1 locus from 11 soybean lines and cDNA of Forrest, Essex, Williams 82 and PI 88788 were fully sequenced. Pairwise sequence alignment revealed seven SNPs/insertion/deletions (InDels), five in the 6th exon and two in the last exon. Using the same 27 soybean lines, we identified one SNP that can be used to select the Rhg1 resistance allele and another SNP that can be employed to differentiate Peking and PI 88788-type resistance. These SNP markers have been validated and a strong correlation was observed between the SNP genotypes and reactions to SCN race 3 using a panel of 153 soybean lines, as well as a bi-parental population, F₅–derived recombinant inbred lines (RILs) from G00-3213 x LG04-6000.

Conclusions

Three functional SNP markers (two for Rhg1 locus and one for Rhg4 locus) were identified that could provide genotype information for the selection of SCN resistance and differentiate Peking from PI 88788 source for most germplasm lines. The robust KASP SNP marker assays were developed. In most contexts, use of one or two of these markers is sufficient for high-throughput marker-assisted selection of plants that will exhibit SCN resistance.

Electronic supplementary material

The online version of this article (doi:10.1186/s12864-015-1531-3) contains supplementary material, which is available to authorized users.     

QTL analysis of cotton fiber length in advanced backcross populations derived from a cross between <Emphasis Type="Italic">Gossypium hirsutum</Emphasis> and <Emphasis Type="Italic">G. mustelinum</Emphasis>

Key message

QTLs for fiber length mapped in three generations of advanced backcross populations derived from crossing Gossypium hirsutum and Gossypium mustelinum showed opportunities to improve elite cottons by introgression from wild relatives.

Abstract

The molecular basis of cotton fiber length in crosses between Gossypium hirsutum and Gossypium mustelinum was dissected using 21 BC₃F₂ and 12 corresponding BC₃F_2:3 and BC₃F_2:4 families. Sixty-five quantitative trait loci (QTLs) were detected by one-way analysis of variance. The QTL numbers detected for upper-half mean length (UHM), fiber uniformity index (UI), and short fiber content (SFC) were 19, 20, and 26 respectively. Twenty-three of the 65 QTLs could be detected at least twice near adjacent markers in the same family or near the same markers across different families/generations, and 32 QTLs were detected in both one-way variance analyses and mixed model-based composite interval mapping. G. mustelinum alleles increased UHM and UI and decreased SFC for five, one, and one QTLs, respectively. In addition to the main-effect QTLs, 17 epistatic QTLs were detected which helped to elucidate the genetic basis of cotton fiber length. Significant among-family genotypic effects were detected at 18, 16, and 16 loci for UHM, UI, and SFC, respectively. Six, two, and two loci showed genotype?×?family interaction for UHM, UI and SFC, respectively, illustrating complexities that might be faced in introgression of exotic germplasm into cultivated cotton. Co-location of many QTLs for UHM, UI, and SFC accounted for correlations among these traits, and selection of these QTLs may improve the three traits simultaneously. The simple sequence repeat (SSR) markers associated with G. mustelinum QTLs will assist breeders in transferring and maintaining valuable traits from this exotic source during cultivar development.

     

Identification and fine mapping of <Emphasis Type="Italic">qWBPH11</Emphasis> conferring resistance to whitebacked planthopper (<Emphasis Type="Italic">Sogatella furcifera</Emphasis> Horvath) in rice (<Emphasis Type="Italic">Oryza sativa</Emphasis> L.)

The whitebacked planthopper (WBPH), Sogatella furcifera Horvath, is one of the most destructive pests in rice (Oryza sativa L.) production. Host-plant resistance has been considered as an efficient and eco-friendly strategy to reduce yield losses caused by WBPH. In this study, we found that an indica rice cultivar IR54751-2-44-15-24-2 (IR54751) displayed high resistance to WBPH at both seedling and tillering stages. The resistance of IR54751 was mainly contributed by antixenosis and tolerance rather than antibiosis. An F₂ population derived from a cross between IR54751 and a susceptible japonica cultivar 02428 was constructed to detect the quantitative trait loci (QTLs) conferring the resistance to WBPH. In total, four QTLs including qWBPH3.1, qWBPH3.2, qWBPH11, and qWBPH12 were identified and distributed on three different chromosomes. The four QTLs had LOD scores of 3.8, 8.2, 5.8, and 3.9, accounting for 8.2, 21.5, 13.9, and 10.4% of the phenotypic variation, respectively. Except for qWBPH3.1, the resistance alleles of the other three QTLs were all from IR54751. Further, a secondary population harboring only single qWBPH11 locus was developed from the F₂ population by marker-assisted selection. Finally, qWBPH11 was delimited in a 450-kb region between markers DJ53973 and SNP56. The identification of WBPH resistance QTLs and the fine mapping of qWBPH11 will be helpful for cloning resistance genes and breeding resistant rice cultivars.     

Mapping quantitative trait loci for root development under hypoxia conditions in soybean (<Emphasis Type="Italic">Glycine max</Emphasis> L. Merr.)

Key message

Greatest potential, QTLs for hypoxia and waterlogging tolerance in soybean roots were detected using a new phenotypic evaluation method.

Abstract

Waterlogging is a major environmental stress limiting soybean yield in wet parts of the world. Root development is an important indicator of hypoxia tolerance in soybean. However, little is known about the genetic control of root development under hypoxia. This study was conducted to identify quantitative trait loci (QTLs) responsible for root development under hypoxia. Recombinant inbred lines (RILs) developed from a cross between a hypoxia-sensitive cultivar, Tachinagaha, and a tolerant landrace, Iyodaizu, were used. Seedlings were subjected to hypoxia, and root development was evaluated with the value change in root traits between after and before treatments. We found 230 polymorphic markers spanning 2519.2 cM distributed on all 20 chromosomes (Chrs.). Using these, we found 11 QTLs for root length (RL), root length development (RLD), root surface area (RSA), root surface area development (RSAD), root diameter (RD), and change in average root diameter (CARD) on Chrs. 11, 12, 13 and 14, and 7 QTLs for hypoxia tolerance of these root traits. These included QTLs for RLD and RSAD between markers Satt052 and Satt302 on Chr. 12, which are important markers of hypoxia tolerance in soybean; those QTLs were stable between 2 years. To validate the QTLs, we developed a near-isogenic line with the QTL region derived from Iyodaizu. The line performed well under both hypoxia and waterlogging, suggesting that the region contains one or more genes with large effects on root development. These findings may be useful for fine mapping and positional cloning of gene responsible for root development under hypoxia.

     

Interactions between <Emphasis Type="Italic">Glu-1</Emphasis> and <Emphasis Type="Italic">Glu-3</Emphasis> loci and associations of selected molecular markers with quality traits in winter wheat (<Emphasis Type="Italic">Triticum aestivum</Emphasis> L.) DH lines

The quality of wheat depends on a large complex of genes and environmental factors. The objective of this study was to identify quantitative trait loci controlling technological quality traits and their stability across environments, and to assess the impact of interaction between alleles at loci Glu-1 and Glu-3 on grain quality. DH lines were evaluated in field experiments over a period of 4 years, and genotyped using simple sequence repeat markers. Lines were analysed for grain yield (GY), thousand grain weight (TGW), protein content (PC), starch content (SC), wet gluten content (WG), Zeleny sedimentation value (ZS), alveograph parameter W (APW), hectolitre weight (HW), and grain hardness (GH). A number of QTLs for these traits were identified in all chromosome groups. The Glu-D1 locus influenced TGW, PC, SC, WG, ZS, APW, GH, while locus Glu-B1 affected only PC, ZS, and WG. Most important marker-trait associations were found on chromosomes 1D and 5D. Significant effects of interaction between Glu-1 and Glu-3 loci on technological properties were recorded, and in all types of this interaction positive effects of Glu-D1 locus on grain quality were observed, whereas effects of Glu-B1 locus depended on alleles at Glu-3 loci. Effects of Glu-A3 and Glu-D3 loci per se were not significant, while their interaction with alleles present at other loci encoding HMW and LMW were important. These results indicate that selection of wheat genotypes with predicted good bread-making properties should be based on the allelic composition both in Glu-1 and Glu-3 loci, and confirm the predominant effect of Glu-D1d allele on technological properties of wheat grains.     

Genome-wide association mapping of quantitative resistance to sudden death syndrome in soybean

Background

Sudden death syndrome (SDS) is a serious threat to soybean production that can be managed with host plant resistance. To dissect the genetic architecture of quantitative resistance to the disease in soybean, two independent association panels of elite soybean cultivars, consisting of 392 and 300 unique accessions, respectively, were evaluated for SDS resistance in multiple environments and years. The two association panels were genotyped with 52,041 and 5,361 single nucleotide polymorphisms (SNPs), respectively. Genome-wide association mapping was carried out using a mixed linear model that accounted for population structure and cryptic relatedness.

Result

A total of 20 loci underlying SDS resistance were identified in the two independent studies, including 7 loci localized in previously mapped QTL intervals and 13 novel loci. One strong peak of association on chromosome 18, associated with all disease assessment criteria across the two panels, spanned a physical region of 1.2 Mb around a previously cloned SDS resistance gene (GmRLK18-1) in locus Rfs2. An additional variant independently associated with SDS resistance was also found in this genomic region. Other peaks were within, or close to, sequences annotated as homologous to genes previously shown to be involved in plant disease resistance. The identified loci explained an average of 54.5% of the phenotypic variance measured by different disease assessment criteria.

Conclusions

This study identified multiple novel loci and refined the map locations of known loci related to SDS resistance. These insights into the genetic basis of SDS resistance can now be used to further enhance durable resistance to SDS in soybean. Additionally, the associations identified here provide a basis for further efforts to pinpoint causal variants and to clarify how the implicated genes affect SDS resistance in soybean.

Electronic supplementary material

The online version of this article (doi:10.1186/1471-2164-15-809) contains supplementary material, which is available to authorized users.     

Mapping novel aphid resistance QTL from wild soybean, <Emphasis Type="Italic">Glycine soja</Emphasis> 85-32

Key message

Two novel QTLs conferring aphid resistance were mapped and validated on soybean chromosomes 8 and 16, respectively. Closely linked markers were developed to assist breeding for aphid resistance.

Abstract

Soybean aphid, Aphis glycines Matsumura, is a highly destructive pest for soybean production. E08934, a soybean advanced breeding line derived from the wild soybean Glycine soja 85-32, has shown strong resistance to aphids. To dissect the genetic basis of aphid resistance in E08934, a mapping population (070020) consisting of 140 F₃-derived lines was developed by crossing E08934 with an aphid-susceptible line E00003. This mapping population was evaluated for aphid resistance in a greenhouse trial in 2010 and three field trials in 2009, 2010, and 2011, respectively. The broad-sense heritability across the field trials was 0.84. In the mapping population 070020, two major quantitative trait loci (QTL) were detected as significantly associated with aphid resistance, and designated as Rag6 and Rag3c, respectively. Rag6 was mapped to a 10.5 centiMorgan (cM) interval between markers MSUSNP08-2 and Satt209 on chromosome 8, explaining 19.5–46.4% of the phenotypic variance in different trials. Rag3c was located at a 7.5 cM interval between markers MSUSNP16-10 and Sat_370 on chromosome 16, explaining 12.5–22.9% of the phenotypic variance in different trials. Rag3c had less resistance effect than Rag6 across all the trials. Furthermore, Rag6 and Rag3c were confirmed in two validation populations with different genetic backgrounds. No significant interaction was detected between Rag6 and Rag3c in either the mapping population or the validation populations. Both Rag6 and Rag3c were indicated as conferring antibiosis resistance to aphids by a no-choice test. The new aphid-resistance gene(s) derived from the wild germplasm G. soja 85-32 are valuable in improving soybeans for aphid resistance.

     

Genetic analysis of shoot fresh weight in a cross of wild (<Emphasis Type="Italic">G. soja</Emphasis>) and cultivated (<Emphasis Type="Italic">G. max</Emphasis>) soybean

Shoot fresh weight (SFW) is one of the parameters, used to estimate the total plant biomass yield in soybean. In the present study, a total of 188 F_5:8 recombinant inbred lines (RIL) derived from an interspecific cross of PI 483463 (Glycine soja) and Hutcheson (Glycine max) were investigated for SFW variation in the field for three consecutive years. The parental lines and RILs were phenotyped in the field at the R6 stage by measuring total biomass in kg/plot to identify the QTLs for SFW. Three QTLs qSFW6_1, qSFW15_1, and qSFW19_1 influencing SFW were identified on chromosome 6, 15, and 19, respectively. The QTL qSFW19_1 flanked between the markers BARC-044913-08839 and BARC-029975-06765 was the stable QTL expressed in all the three environments. The phenotypic variation explained by the QTLs across all environments ranged from 6.56 to 21.32 %. The additive effects indicated contribution of alleles from both the parents and additive × environment interaction effects affected the expression of SFW QTL. Screening of the RIL population with additional SSRs from the qSFW19_1 region delimited the QTL between the markers SSR19-1329 and BARC-29975-06765. QTL mapping using bin map detected two QTLs, qSFW19_1A and qSFW19_1B. The QTL qSFW19_1A mapped close to the Dt1 gene locus, which affects stem termination, plant height, and floral initiation in soybean. Potential candidate genes for SFW were pinpointed, and sequence variations within their sequences were detected using high-quality whole-genome resequencing data. The findings in this study could be useful for understanding genetic basis of SFW in soybean.     

Genome-wide association study for soybean cyst nematode resistance in Chinese elite soybean cultivars

Soybean cyst nematode (SCN) (Heterodera glycines Ichinohe) is a highly recalcitrant endoparasite of soybean roots, causing more yield loss than any other pest. To identify quantitative trait loci (QTL) controlling resistance to SCN (HG type 2.5.7, race 1), a genome-wide association study (GWAS) was performed. The association panel, consisting of 120 Chinese soybean cultivars, was genotyped with 7189 single nucleotide polymorphism (SNPs). A total of 6204 SNPs with minor allele frequency >0.05 were used to estimate linkage disequilibrium (LD) and population structure. The mean level of LD measured by r ² declined very rapidly to half its maximum value (0.51) at 220 kb. The overall population structure was approximately coincident with geographic origin. The GWAS results identified 13 SNPs in 7 different genomic regions significantly associated with SCN resistance. Of these, three SNPs were localized in previously mapped QTL intervals, including rhg1 and Rhg4. The GWAS results also detected 10 SNPs in 5 different genomic regions associated with SCN resistance. The identified loci explained an average of 95.5% of the phenotypic variance. The proportion of phenotypic variance was due to additive genetic variance of the validated SNPs. The present study identified multiple new loci and refined chromosomal regions of known loci associated with SCN resistance. The loci and trait-associated SNPs identified in this study can be used for developing soybean cultivars with durable resistance against SCN.     

Detecting the QTL-allele system conferring flowering date in a nested association mapping population of soybean using a novel procedure

Key message

The RTM-GWAS was chosen among five procedures to identify DTF QTL-allele constitution in a soybean NAM population; 139 QTLs with 496 alleles accounting for 81.7% of phenotypic variance were detected.

Abstract

Flowering date (days to flowering, DTF) is an ecological trait in soybean, closely related to its ability to adapt to areas. A nested association mapping (NAM) population consisting of four RIL populations (LM, ZM, MT and MW with M8206 as their common parent) was established and tested for their DTF under five environments. Using restriction-site-associated DNA sequencing the population was genotyped with SNP markers. The restricted two-stage multi-locus (RTM) genome-wide association study (GWAS) (RTM-GWAS) with SNP linkage disequilibrium block (SNPLDB) as multi-allele genomic markers performed the best among the five mapping procedures with software publicly available. It identified the greatest number of quantitative trait loci (QTLs) (139) and alleles (496) on 20 chromosomes covering almost all of the QTLs detected by four other mapping procedures. The RTM-GWAS provided the detected QTLs with highest genetic contribution but without overflowing and missing heritability problems (81.7% genetic contribution vs. heritability of 97.6%), while SNPLDB markers matched the NAM population property of multiple alleles per locus. The 139 QTLs with 496 alleles were organized into a QTL-allele matrix, showing the corresponding DTF genetic architecture of the five parents and the NAM population. All lines and parents comprised both positive and negative alleles, implying a great potential of recombination for early and late DTF improvement. From the detected QTL-allele system, 126 candidate genes were annotated and χ ² tested as a DTF candidate gene system involving nine biological processes, indicating the trait a complex, involving several biological processes rather than only a handful of major genes.

     

Construction of a genome-anchored,high-density genetic map for melon (<Emphasis Type="Italic">Cucumis melo</Emphasis> L.) and identification of <Emphasis Type="Italic">Fusarium oxysporum</Emphasis> f. sp. <Emphasis Type="Italic">melonis</Emphasis> race 1 resistance QTL

Key message

Four QTLs and an epistatic interaction were associated with disease severity in response to inoculation with Fusarium oxysporum f. sp. melonis race 1 in a recombinant inbred line population of melon.

Abstract

The USDA Cucumis melo inbred line, MR-1, harbors a wealth of alleles associated with resistance to several major diseases of melon, including powdery mildew, downy mildew, Alternaria leaf blight, and Fusarium wilt. MR-1 was crossed to an Israeli cultivar, Ananas Yok’neam, which is susceptible to all of these diseases, to generate a recombinant inbred line (RIL) population of 172 lines. In this study, the RIL population was genotyped to construct an ultra-dense genetic linkage map with 5663 binned SNPs anchored to the C. melo genome and exhibits the overall high quality of the assembly. The utility of the densely genotyped population was demonstrated through QTL mapping of a well-studied trait, resistance to Fusarium wilt caused by Fusarium oxysporum f. sp. melonis (Fom) race 1. A major QTL co-located with the previously validated resistance gene Fom-2. In addition, three minor QTLs and an epistatic interaction contributing to Fom race 1 resistance were identified. The MR-1 × AY RIL population provides a valuable resource for future QTL mapping studies and marker-assisted selection of disease resistance in melon.

     

Identification of candidate genes of QTLs for seed weight in <Emphasis Type="Italic">Brassica napus</Emphasis> through comparative mapping among <Emphasis Type="Italic">Arabidopsis</Emphasis> and <Emphasis Type="Italic">Brassica</Emphasis>species

Background

Map-based cloning of quantitative trait loci (QTLs) in polyploidy crop species remains a challenge due to the complexity of their genome structures. QTLs for seed weight in B. napus have been identified, but information on candidate genes for identified QTLs of this important trait is still rare.

Results

In this study, a whole genome genetic linkage map for B. napus was constructed using simple sequence repeat (SSR) markers that covered a genetic distance of 2,126.4 cM with an average distance of 5.36 cM between markers. A procedure was developed to establish colinearity of SSR loci on B. napus with its two progenitor diploid species B. rapa and B. oleracea through extensive bioinformatics analysis. With the aid of B. rapa and B. oleracea genome sequences, the 421 homologous colinear loci deduced from the SSR loci of B. napus were shown to correspond to 398 homologous loci in Arabidopsis thaliana. Through comparative mapping of Arabidopsis and the three Brassica species, 227 homologous genes for seed size/weight were mapped on the B. napus genetic map, establishing the genetic bases for the important agronomic trait in this amphidiploid species. Furthermore, 12 candidate genes underlying 8 QTLs for seed weight were identified, and a gene-specific marker for BnAP2 was developed through molecular cloning using the seed weight/size gene distribution map in B. napus.

Conclusions

Our study showed that it is feasible to identify candidate genes of QTLs using a SSR-based B. napus genetic map through comparative mapping among Arabidopsis and B. napus and its two progenitor species B. rapa and B. oleracea. Identification of candidate genes for seed weight in amphidiploid B. napus will accelerate the process of isolating the mapped QTLs for this important trait, and this approach may be useful for QTL identification of other traits of agronomic significance.

     

QTL mapping for resistance to Ceratocystis wilt in <Emphasis Type="Italic">Eucalyptus</Emphasis>

Ceratocystis wilt caused by the fungus Ceratocystis fimbriata, is currently one of the major diseases in commercial plantations of Eucalyptus trees in Brazil. Deployment of resistant genotypes has been the main strategy for effective disease management. The present study aimed at identifying genomic regions underlying the genetic control of resistance to Ceratocystis wilt in Eucalyptus by quantitative trait loci (QTL) mapping in an outbred hybrid progeny derived from a cross between (Eucalyptus dunnii × Eucalyptus grandis) × (Eucalyptus urophylla × Eucalyptus globulus). A segregating population of 127 individuals was phenotyped for resistance to Ceratocystis wilt using controlled inoculation under a completely randomized design with five clonal replicates per individual plant. The phenotypic resistance response followed a continuous variation, enabling us to analyze the trait in a quantitative manner. The population was genotyped with 114 microsatellite markers and 110 were mapped with an average interval of 12.3 cM. Using a sib-pair interval-mapping approach five QTLs were identified for disease resistance, located on linkage groups 1, 3, 5, 8, and 10, and their estimated individual heritability ranged from 0.096 to 0.342. The QTL on linkage group 3 overlaps with other fungal disease-resistance QTLs mapped earlier and is consistent with the annotation of several disease-resistance genes on this chromosome in the E. grandis genome. This is the first study to identify and attempt to quantify the effects of QTLs associated with resistance to Ceratocystis wilt in Eucalyptus.     

A first step toward the development of a barley NAM population and its utilization to detect QTLs conferring leaf rust seedling resistance

Key message

We suggest multi-parental nested association mapping as a valuable innovation in barley genetics, which increases the power to map quantitative trait loci and assists in extending genetic diversity of the elite barley gene pool.

Abstract

Plant genetic resources are a key asset to further improve crop species. The nested association mapping (NAM) approach was introduced to identify favorable genes in multi-parental populations. Here, we report toward the development of the first explorative barley NAM population and demonstrate its usefulness in a study on mapping quantitative trait loci (QTLs) for leaf rust resistance. The NAM population HEB-5 was developed from crossing and backcrossing five exotic barley donors with the elite barley cultivar ‘Barke,’ resulting in 295 NAM lines in generation BC₁S₁. HEB-5 was genetically characterized with 1,536 barley SNPs. Across HEB-5 and within the NAM families, no deviation from the expected genotype and allele frequencies was detected. Genetic similarity between ‘Barke’ and the NAM families ranged from 78.6 to 83.1 %, confirming the backcrossing step during population development. To explore its usefulness, a screen for leaf rust (Puccinia hordei) seedling resistance was conducted. Resistance QTLs were mapped to six barley chromosomes, applying a mixed model genome-wide association study. In total, four leaf rust QTLs were detected across HEB-5 and four QTLs within family HEB-F23. Favorable exotic QTL alleles reduced leaf rust symptoms on two chromosomes by 33.3 and 36.2 %, respectively. The located QTLs may represent new resistance loci or correspond to new alleles of known resistance genes. We conclude that the exploratory population HEB-5 can be applied to mapping and utilizing exotic QTL alleles of agronomic importance. The NAM concept will foster the evaluation of the genetic diversity, which is present in our primary barley gene pool.     

Mapping of new quantitative trait loci for sudden death syndrome and soybean cyst nematode resistance in two soybean populations

Key message

Novel QTL conferring resistance to both the SDS and SCN was detected in two RIL populations. Dual resistant RILs could be used in breeding programs for developing resistant soybean cultivars.

Abstract

Soybean cultivars, susceptible to the fungus Fusarium virguliforme, which causes sudden death syndrome (SDS), and to the soybean cyst nematode (SCN) (Heterodera glycines), suffer yield losses valued over a billion dollars annually. Both pathogens may occur in the same production fields. Planting of cultivars genetically resistant to both pathogens is considered one of the most effective means to control the two pathogens. The objective of the study was to map quantitative trait loci (QTL) underlying SDS and SCN resistances. Two recombinant inbred line (RIL) populations were developed by crossing ‘A95-684043’, a high-yielding maturity group (MG) II line resistant to SCN, with ‘LS94-3207’ and ‘LS98-0582’ of MG IV, resistant to both F. virguliforme and SCN. Two hundred F₇ derived recombinant inbred lines from each population AX19286 (A95-684043 × LS94-3207) and AX19287 (A95-684043 × LS98-0582) were screened for resistance to each pathogen under greenhouse conditions. Five hundred and eighty and 371 SNP markers were used for mapping resistance QTL in each population. In AX19286, one novel SCN resistance QTL was mapped to chromosome 8. In AX19287, one novel SDS resistance QTL was mapped to chromosome 17 and one novel SCN resistance QTL was mapped to chromosome 11. Previously identified additional SDS and SCN resistance QTL were also detected in the study. Lines possessing superior resistance to both pathogens were also identified and could be used as germplasm sources for breeding SDS- and SCN-resistant soybean cultivars.

     

Discovery of a seventh <Emphasis Type="Italic">Rpp</Emphasis> soybean rust resistance locus in soybean accession PI 605823

Key message

A novel Rpp gene from PI 605823 for resistance to Phakopsora pachyrhizi was mapped on chromosome 19.

Abstract

Soybean rust, caused by the obligate biotrophic fungal pathogen Phakopsora pachyrhizi Syd. & P. Syd, is a disease threat to soybean production in regions of the world with mild winters. Host plant resistance conditioned by resistance to P. pachyrhizi (Rpp) genes has been found in numerous soybean accessions, and at least 10 Rpp genes or alleles have been mapped to six genetic loci. Identifying additional disease-resistance genes will facilitate development of soybean cultivars with durable resistance. PI 605823, a plant introduction from Vietnam, was previously identified as resistant to US populations of P. pachyrhizi in greenhouse and field trials. In this study, bulked segregant analysis using an F₂ population derived from ‘Williams 82’ × PI 605823 identified a genomic region associated with resistance to P. pachyrhizi isolate GA12, which had been collected in the US State of Georgia in 2012. To further map the resistance locus, linkage mapping was carried out using single-nucleotide polymorphism markers and phenotypic data from greenhouse assays with an F_2:3 population derived from Williams 82 × PI 605823 and an F_4:5 population derived from ‘5601T’ × PI 605823. A novel resistance gene, Rpp7, was mapped to a 154-kb interval (Gm19: 39,462,291–39,616,643 Glyma.Wm82.a2) on chromosome 19 that is different from the genomic locations of any previously reported Rpp genes. This new gene could be incorporated into elite breeding lines to help provide more durable resistance to soybean rust.

     

Identification of Novel Strain-Specific and Environment-Dependent Minor QTLs Linked to Fire Blight Resistance in Apples

Since its first report almost 200 years ago, fire blight, caused by the gram-negative bacterium Erwinia amylovora, has threatened apple and pear production globally. Identifying novel genes and their functional alleles is a prerequisite to developing apple cultivars with enhanced fire blight resistance. Here, we report 13 strain-specific and environment-dependent minor QTLs linked to fire blight resistance from a segregating Malus sieversii × Malus × domestica mapping population. Interval mapping at 95% confidence and Kruskal–Wallis analysis at P value =?0.005 were used to identify QTLs for three strains of E. amylovora differing in virulence and pathogenicity. The QTLs identified explain a small to moderate part of resistance variability, and a majority was not common between years or E. amylovora strains. These QTLs are distributed in eight linkage groups of apples and comparison of their map position to previously identified fire blight resistance QTLs indicates that most are novel loci. Interaction between experimental conditions in the greenhouse and field, and between years, and differences in virulence levels of strains might be responsible for strain- and year-specific QTLs. The QTLs identified on LG10 for strain Ea273 in 2011 and strain LP101 in 2011, and on LG15 for strain LP101 could be the same QTLs identified previously with strain CFBP1430 in cultivar “Florina” and “Co-op16 × Co-op17” mapping population, respectively. We discuss the potential impact of newly identified minor fire blight QTLs and major gene-based resistance on the rate of mutation in pathogen populations to overcome resistance and durability of resistance.