Molecular markers linked to rhizomania resistance in sugar beet, Beta vulgaris, from two different sources map to the same linkage group

Rhizomania, one of the most important diseases of sugar beet, is caused by beet necrotic yellow vein virus, a Furovirus vectored by the fungus Polymyxa betae Keskin. Reduction of the production losses caused by this disease can only be achieved by using tolerant cultivars. The objective of this study was the identification and mapping of random amplified polymorphic DNA (RAPD) markers linked to a rhizomania resistance gene. The RAPD markers were identified using bulked segregant analysis in a segregating population of 62 individuals derived by intercrossing plants of the resistant commercial hybrid GOLF, and the resistance locus was positioned in a molecular marker linkage map made with a different population of 50 GOLF plants. The resistance locus, Rr1, was mapped to linkage group III of our map of Beta vulgaris L. ssp. vulgaris, which consisted of 76 RAPDs, 20 restriction fragment length polymorphisms (RFLPs), three sequence characterized amplified regions (SCARs) and one sequence tagged site (STS). In total, 101 molecular markers were mapped over 14 linkage groups which spanned 688.4 cM with an average interval length of 8.0 cM. In the combined map, Rr1 proved to be flanked by the RAPD loci RA411₁₈₀₀ and AS7₁₁₀₀ at 9.5 and 18.5cM, respectively. Moreover, in our I₂ population, we found that a set of markers shown by Barzen et al. (1997) to be linked to the ‘Holly’ type resistance gene was also linked to the ‘GOLF’-type resistance gene. These results appeared to indicate that the rhizomania resistance gene present in the GOLF hybrid could be the same gene underlying resistance in ‘Holly’-based resistant genotypes. Two other explanations could be applied: first, that two different alleles at the same locus could have been selected; second, that two different genes at two different but clustered loci underwent the selection process.     

Mapping of quantitative trait loci controlling partial resistance against rust incited by <Emphasis Type="Italic">Uromyces pisi</Emphasis> (Pers.) Wint. in a <Emphasis Type="Italic">Pisum fulvum</Emphasis> L. intraspecific cross

A quantitative trait loci (QTL) associated with resistance to pea rust, caused by the fungus Uromyces pisi (Pers.) Wint., has been identified in a F₂ population derived from an intraspecific cross between two wild pea (Pisum fulvum L.) accessions, IFPI3260 (resistant) and IFPI3251 (susceptible). Both parental lines and all the segregating population displayed a fully compatible interaction (high infection type), which indicates absence of hypersensitive response. Nevertheless, differences on the percentage of symptomatic area of the whole plant (disease severity) were observed. A genetic map was developed covering 1283.3 cM and including 146 markers (144 random amplified polymorphic DNA (RAPDs) and two sequence tagged sites (STSs) markers) distributed in 9 linkage groups. A QTL explaining 63% of the total phenotypic variation was located in linkage group 3. RAPDs markers (OPY11₁₃₁₆ and OPV17₁₀₇₈) flanking this QTL should allow, after their conversion in SCARs, a reliable marker-assisted selection for rust resistance.     

Genetic analysis of resistance to barley scald (Rhynchosporium secalis) in the Ethiopian line `Abyssinian' (CI668)

A doubled haploid barley (Hordeum vulgare L.) population from a cross between the cultivar `Ingrid' and the Ethiopian landrace `Abyssinian' was mapped by AFLP, RFLP, SSR and STS markers and tested for resistance to isolates`4004', `2', `16-6', `17', `22' and `WRS 1872' of Rhynchosporium secalis (Oudem.) J.J. Davis, the causal agent of leaf scald. Resistance tests were conducted on parents, DH-lines, a near-isogenic line of `Abyssinian' (NIL) into `Ingrid', and an F₂ population descended from the same F₁ plants as the DHs. The DH population segregated for at least two major R. secalis resistance QTL. All isolates tested identified a major QTL on chromosome 3 (3H) associated with R. secalis resistance, in a 4 cM support interval between the co-segregating markers Bmac0209/Falc666 and MWG680. The QTL was linked with the markers Falc666 (2.3 cM), YLM/ylp (0.3 cM), MWG680 (1.7 cM), cttaca2 (2.5 cM) and agtc17 (9.8 cM). The second QTL was located on chromosome 1 (7H).However, this QTL was only detected by one isolate and was located in an interval of 16 cM in the distal part of the chromosome. At this QTL the allele for improved scald resistance originated from the parent `Ingrid'. There were a number of minor QTL on chromosomes 2 (2H), 4 (4H) and 6 (6H) that were not repeatable either across replications or analysis methods. The importance of checking QTL-models by cross-validation is stressed. This revised version was published online in August 2006 with corrections to the Cover Date.     

Linkage map construction and mapping QTL for cotton fibre quality using SRAP, SSR and RAPD

Tetraploid cotton is one of the most extensively cultivated species. Two tetraploid species, Gossypium hirsutum L. and G. barbadense L., dominate the world's cotton production. To better understand the genetic basis of cotton fibre traits for the improvement of fibre quality, a genetic linkage map of tetraploid cotton was constructed using sequence‐related amplified polymorphisms (SRAPs), simple sequence repeats (SSRs) and random amplified polymorphic DNAs (RAPDs). A total of 238 SRAP primer combinations, 368 SSR primer pairs and 600 RAPD primers were used to screen polymorphisms between G. hirsutum cv. Handan208 and G. barbadense cv. Pima90 which revealed 749 polymorphic loci in total (205 SSRs, 107 RAPDs and 437 SRAPs). Sixty‐nine F₂ progeny from the interspecific cross of ‘Handan208’בPima90’ were genotyped with the 749 polymorphic markers. A total of 566 loci were assembled into 41 linkage groups with at least three loci in each group. Twenty‐eight linkage groups were assigned to corresponding chromosomes by SSR markers with known chromosome locations. The map covered 5141.8 cM with a mean interlocus space of 9.08 cM. A × test for significance of deviations from the expected ratio (1: 2: 1 or 3: 1) identified 135 loci (18.0%) with skewed segregation, most of which had an excess of maternal parental alleles. In total, 13 QTL associated with fibre traits were detected, among which two QTL were for fibre strength, four for fibre length and seven for micronaire value. These QTL were on nine linkage groups explaining 16.18‐28.92% of the trait variation. Six QTL were located in the A subgenome, six QTL in the D subgenome and one QTL in an unassigned linkage group. There were three QTL for micronaire value clustered on LG1, which would be very useful for improving this trait by molecular marker‐assisted selection.     

Molecular mapping of Aegilops speltoides derived leaf rust resistance gene Lr28 in wheat

In a segregating homozygous F₂ population of bread wheat involving a leaf rust resistance gene Lr28 derived from Aegilops speltoides, six randomly amplified polymorphic DNA (RAPD) markers, three each in coupling and repulsion phase were identified as linked to Lr28, mapped to a region spanning 32 cM including the locus. The F₂ and F₃ populations were studied in the phytotron challenged with the most virulent pathotype 77-5 of leaf rust. A coupling phase linked RAPD marker S464₇₂₁ and a repulsion phase linked RAPD marker S326₅₅₀ flanked the gene Lr28 by a distance of 2.4± 0.016 cM on either side. The flanking markers genetically worked as co-dominant markers when analyzed together after separate amplification in the F₂ population by distinguishing the homozygotes from the heterozygotes and increased the efficiency of marker assisted selection by reducing the false positives and negatives. One of the three RAPD markers, S421₆₄₀ was converted to locus specific SCAR marker SCS421₆₄₀ which was further truncated by designing primers internal from both ends of the original RAPD amplicon to eliminate a non-specific amplification of nearly same size. The truncated polymorphic sequence characterized amplified region marker (TPSCAR) SCS421₅₇₀ was 70 bp smaller, but resulted in a single band polymorphism specific to Lr28 resistance. The TPSCAR marker was validated for its specificity to the gene Lr28 in nine different genetic backgrounds and on 43 of the 50 Lr genes of both native and alien origin, suggesting the utility of the SCAR markers in pyramiding leaf rust resistance genes in wheat.     

Identification of SSR markers linked to the Phytophthora resistance gene Rps1-d in soybean

To identify markers for the Phytophthora resistance gene, Rps1‐d, 123 F_{2 : 3} families were produced from a cross between Glycine max (L.) Merr. ‘Tanbakuro’ (a Japanese traditional black soybean) and PI103091 (Rps1‐d) as an experimental population. The results of virulence tests produced 33 homozygous resistant, 61 segregating and 29 homozygous susceptible F_{2 : 3} families. The chi‐squared test gave a goodness‐of‐fit for the expected ratio of 1 : 2 : 1 for resistant, segregating and susceptible traits, suggesting that the inheritance of Rps1‐d is controlled by a monogenic dominant gene. Simple sequence repeat (SSR) analyses of this trait were carried out using the cultivars ‘Tanbakuro’ and PI103091. Sixteen SSR primers, which produced 19 polymorphic fragments between the two parents, were identified from 41 SSR primers in MLG N. Eight SSR markers were related to Rps1‐d, based on 32 of the 123 F_{2 : 3} families, consisting of 16 homozygous resistant and 16 homozygous susceptible lines. The remaining 91 families were analysed for these eight markers, and a linkage map was constructed using all 123 F_{2 : 3} families. The length of this linkage group is 44.0 cM. The closest markers, Sat_186 and Satt152, are mapped at 5.7 cM and 11.5 cM, respectively, on either side of the Rps1‐d gene. Three‐way contingency table analysis indicates that dual‐marker‐assisted selection using these two flanking markers would be efficient.     

Quantitative trait loci mapping of seed colour,hairy leaf,seedling anthocyanin,leaf chlorosis and days to flowering in F2 population of Brassica rapa L.

A diversity arrays technology (DArT) map was constructed to identify quantitative trait loci (QTL) affecting seed colour, hairy leaf, seedling anthocyanin, leaf chlorosis and days to flowering in Brassica rapa using a F₂ population from a cross between two parents with contrasting traits. Two genes with dominant epistatic interaction were responsible for seed colour. One major dominant gene controls the hairy leaf trait. Seedling anthocyanin was controlled by a major single dominant gene. The parents did not exhibit leaf chlorosis; however, 32% F₂ plants showed leaf chlorosis in the population. A distorted segregation was observed for days to flowering in the F₂ population. A linkage map was constructed with 376 DArT markers distributed over 12 linkage groups covering 579.7 cM. The DArT markers were assigned on different chromosomes of B. rapa using B. rapa genome sequences and DArT consensus map of B. napus. Two QTL (RSC1‐2 and RSC12‐56) located on chromosome A8 and chromosome A9 were identified for seed colour, which explained 19.4% and 18.2% of the phenotypic variation, respectively. The seed colour marker located in the ortholog to Arabidopsis thaliana Transparent Testa2 (AtTT2). Two QTL RLH6‐0 and RLH9‐16 were identified for hairy leaf, which explained 31.6% and 20.7% phenotypic variation, respectively. A single QTL (RSAn‐12‐157) on chromosome A7, which explained 12.8% of phenotypic variation was detected for seedling anthocyanin. The seedling anthocyanin marker is found within the A. thaliana Transparent Testa12 (AtTT12) ortholog. A QTL (RLC6‐04) for leaf chlorosis was identified, which explained 55.3% of phenotypic variation. QTL for hairy leaf and leaf chlorosis were located 0–4 cM apart on the same chromosome A1. A single QTL (RDF‐10‐0) for days to flowering was identified, which explained 21.4% phenotypic variation.     

Construction of high-density linkage map and identification of QTLs associated with resistance to black rot in radish (Raphanus sativus) by RAD sequencing

High-density marker-based QTL mapping can serve as an effective strategy to identify novel genomic information to facilitate crop improvement. In this study, we genotyped an F₂ population (KB12-1 × PP12-1) using a RAD-seq approach and constructed a high-density linkage map for radish. After a series of filtering procedures were performed, 17,124 SNPs and 3,336 indels with aa × bb genotyping were retained to obtain bin markers. Then, a linkage map comprising a total of 1,221 bin markers in nine linkage groups spanning 1,467.3 cM with an average marker interval of 1.2 cM was constructed. We evaluated the resistance of the F₂ mapping population to black rot using F₃ progeny, and two major QTLs related to black rot resistance were identified based on this map. Among these QTLs, qBRR2 on Chr.2 explained 26.97% of the phenotypic variation with a LOD score of 11.93, and qBRR7 on Chr.7 accounted for 27.06% of the phenotypic variation with a LOD score of 11.83. The additive effect of qBRR2 was positive (14.97); however, qBRR7 had the opposite effect (−11.99). The high-density linkage map and the major QTLs qBRR2 and qBRR7 provide new important information for disease resistance gene discovery and utilization in genetic improvement.     

Identification of RAPD markers linked to the rust (<Emphasis Type="Italic">Uromyces fabae</Emphasis>) resistance gene in pea (<Emphasis Type="Italic">Pisum sativum</Emphasis>)

Summary Two RAPD markers linked to gene for resistance (assayed as pustule number cm⁻² leaf area) to rust [Uromyces fabae (Pers.) de Bary] in pea (Pisum sativum L.) were identified using a mapping population of 31 BC₁F₁ [HUVP 1 (HUVP 1 × FC 1] plants, FC 1 being the resistant parent. The analysis of genetics of rust resistance was based on the parents, F₁, F₂, BC₁F₁ and BC₁F₂ generations. Rust resistance in pea is of non-hypersensitive type; it appeared to be governed by a single partially dominant gene for which symbol Ruf is proposed. Further, this trait seems to be affected by some polygenes in addition to the proposed oligogene Ruf. A total of 614 decamer primers were used to survey the parental polymorphism with regard to DNA amplification by polymerase chain reaction. The primers that amplified polymorphic bands present in the resistant parent (FC 1) were used for bulked segregant analysis. Those markers that amplified consistently and differentially in the resistant and susceptible bulks were separately tested with the 31 BC₁F₁ individuals. Two RAPD makers, viz., SC10-82₃₆₀ (primer, GCCGTGAAGT), and SCRI-71₁₀₀₀ (primer, GTGGCGTAGT), flanking the rust resistance gene (Ruf) with a distance of 10.8 cM (0.097 rF and LOD of 5.05) and 24.5 cM (0.194 rF and a LOD of 2.72), respectively, were identified. These RAPD markers were not close enough to Ruf to allow a dependable maker-assisted selection for rust resistance. However, if the two makers flanking Ruf were used together, the effectiveness of MAS would be improved considerably.     

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

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

Molecular characterization of a novel powdery mildew resistance gene Pm30 in wheat originating from wild emmer

Powdery mildew caused by Erysiphe graminis f. sp. tritici is one of the most important wheat diseases in many regions of theworld. A powdery mildew resistance gene, originating from wild emmerwheat (Triticum dicoccoides) accession `C20', from Rosh Pinna, Israel,was successfully transferred to hexaploid wheat through crossing andbackcrossing. Genetic analysis indicated that a single dominant genecontrols the powdery mildew resistance at the seedling stage. SegregatingBC₁F₂ progenies of the cross 87-1/C20//2*8866 wereused for bulked segregant analysis (BSA). The PCR approach was used togenerate polymorphic DNA fragments between the resistant and susceptibleDNA pools by use of 10-mer random primers, STS primers, and wheatmicrosatellite primers. Three markers, Xgwm159/430,Xgwm159/460, and Xgwm159/500, were found to be linked tothe resistance gene. After evaluating the polymorphic markers in twosegregating populations, the distance between the markers and the mildewresistance gene was estimated to be 5–6 cM. By means of ChineseSpring nullisomic-tetrasomics and ditelosomics, the polymorphic markersand the resistance gene were assigned to chromosome arm 5BS and werephysically mapped on the gene rich regions of fragment length (FL) 0.41–0.43 by Chinese Spring deletion lines. As no powdery mildew resistancegene has been reported on chromosome arm 5BS, the mildew resistancegene originating from C20 should be a new gene and is designated Pm30.     

Genetic analysis and identification of SSR marker linked to Phomopsis blight resistance in eggplant (Solanum melongena L.)

The present investigation was carried out to decipher inheritance of resistance and to identify linked SSR markers for Phomopsis blight resistance in eggplant. An F₂ population comprising 161 plants was developed from the cross of Pusa Kranti and BR-40-7. Genetic analysis was carried out using Chi square test. Artificial inoculation of fruits was carried out using pin prick method, and scoring was done as per the standard scoring scale. The F₂ plants segregated into 92 susceptible (77—highly susceptible, 15—susceptible): 69 resistant (17—highly resistant, 27—resistant, 25—moderately resistant) suggesting complimentary epistasis with ratio of 9:7. To identify the putatively linked markers to resistance gene, parental polymorphic markers were subjected to bulk segregant analysis (BSA), and two markers (emk03O04 and emf11A03) could differentiate resistant and susceptible bulk and co-segregated with resistance gene. The genetic distance between the identified markers was found to be 18.12 cM using QTL IciMapping V3.2 software depicting two new QTLs on chromosome number 6. The identified QTLs have great significant importance in marker assisted breeding programme.     

Development of a SCAR marker linked with a MYMV resistance gene in mungbean (Vigna radiata L. Wilczek)

Yellow mosaic disease (YMD) caused by mungbean yellow mosaic virus (MYMV) is the most important disease of mungbean, causing great yield loss. The present investigation was carried out to study the inheritance and identify molecular markers linked with MYMV resistance gene by using F₁, F₂ and 167 F_2 : 8 recombinant inbred lines (RILs) developed from the cross ‘TM‐99‐37’ (resistant) × Mulmarada (susceptible). The F₁ was susceptible, F₂ segregated in 3S:1R phenotypic ratio and RILs segregated in 1S:1R ratio in the field screening indicating that the MYMV resistance gene is governed by a single recessive gene. Of the 140 RAPD primers, 45 primers showing polymorphism in parents were screened using bulked segregant analysis. Three primers amplified specific polymorphic fragments viz. OPB‐07_600, OPC‐06₁₇₅₀ and OPB‐12₈₂₀. The marker OPB‐07₆₀₀ was more closely linked (6.8 cM) with a MYMV resistance gene as compared to OPC‐06₁₇₅₀ (22.8 cM) and OPB‐12₈₂₀ (25.2 cM). The resistance‐specific fragment OPB‐07₆₀₀ was cloned, sequenced and converted into a sequence‐characterized amplified region (SCAR) marker and validated in twenty genotypes with different genetic backgrounds.     

YM型小麦温敏雄性不育系不育基因的QTL定位

YM型小麦温敏雄性不育系的不育基因被定位在1Bs染色体片段上, 但已发现的相邻分子标记与该基因的遗传距离较大, 达10 cM以上。为寻找与该基因连锁更紧密的分子标记, 以YM型温敏雄性不育系ATM3314与恢复系中国春杂交的F₂代200株为作图群体, 从1Bs的22个SSR引物中筛选出5个在亲本和F₂代中分离的SSR引物, 构建了1个包含5个标记的1Bs局部遗传连锁图谱。结合F₂代个体的育性调查, 采用复合区间作图法在YM型温敏雄性不育系的1Bs染色体上检测到不育基因的1个主效QTLrfv1-1和1个微效QTLrfv1-2。rfv1-1位于SSR标记Xgwm18和Xwmc406之间, 与两标记的遗传距离分别为6.0 cM和4.6 cM, LOD值为8.80, 加性效应23.87, 显性效应10.44, 可解释表型变异的23.91%; rfv1-2位于Xwmc406和Xbarc8之间, 与两标记的遗传距离分别为4.0 cM和3.4 cM, LOD值为3.10, 加性效应17.59, 显性效应5.99, 可解释表型变异的7.78%。本研究初步定位了YM型小麦温敏雄性不育系1Bs染色体片段上不育基因的QTL, 为进一步准确定位该基因奠定了基础。     

Mapping and validation of QTLs for resistance to an Indian isolate of Ascochyta blight pathogen in chickpea

Ascochyta blight (AB) caused by Ascochyta rabiei, is globally the most important foliar disease that limits the productivity of chickpea (Cicer arietinum L.). An intraspecific linkage map of cultivated chickpea was constructed using an F₂ population derived from a cross between an AB susceptible parent ICC 4991 (Pb 7) and an AB resistant parent ICCV 04516. The resultant map consisted of 82 simple sequence repeat (SSR) markers and 2 expressed sequence tag (EST) markers covering 10 linkage groups, spanning a distance of 724.4 cM with an average marker density of 1 marker per 8.6 cM. Three quantitative trait loci (QTLs) were identified that contributed to resistance to an Indian isolate of AB, based on the seedling and adult plant reaction. QTL1 was mapped to LG3 linked to marker TR58 and explained 18.6% of the phenotypic variance (R ²) for AB resistance at the adult plant stage. QTL2 and QTL3 were both mapped to LG4 close to four SSR markers and accounted for 7.7% and 9.3%, respectively, of the total phenotypic variance for AB resistance at seedling stage. The SSR markers which flanked the AB QTLs were validated in a half-sib population derived from the same resistant parent ICCV 04516. Markers TA146 and TR20, linked to QTL2 were shown to be significantly associated with AB resistance at the seedling stage in this half-sib population. The markers linked to these QTLs can be utilized in marker-assisted breeding for AB resistance in chickpea.     

Identification of PCR-based markers linked to the powdery-mildew-resistance gene Pl1 from Malus robusta in cultivated apple

The availability of molecular markers linked to mildew resistance genes would enhance the efficiency of apple-breeding programmes. This investigation focuses on the identification of random amplified polymorphic DNA (RAPD) markers linked to the Pl₁ gene for mildew resistance, which has introgressed from Malus robusta into cultivated apples. The RAPD marker technique was combined with a modified ‘bulked seg-regant analysis’ mapping strategy. About 850 random decamer primers used as single primers or in combinations were tested by PCR analysis on the basis of resistant and susceptible DNA pools. Selected primers producing RAPD fragments were applied in an additional selection step to M. robusta and genotypes representing intermediate breeding stages of the breeding population 93/9, for which a 1:1 segregation could be observed for the resistance trait. Seven RAPD markers, all representing introgressed DNA sequences from M. robusta, were identified and arranged with the Pl₁ locus in a common linkage group. The two most tightly-linked RAPD markers, OPAT20₄₅₀ and OPD2₁₀₀₀ were mapped with a genetic distance of 4.5 and 5 cM, respectively, from the Pl₁ gene. Both markers are suitable for marker-assisted selection in apple breeding. The polymorphic DNA fragment OPAT20₄₅₀ was cloned and sequenced, and longer primers for the generation of a sequence-characterized amplified region (SCAR) marker have been constructed; this marker was easier to score than the original RAPD marker.     

Inheritance and molecular mapping of restorer‐of‐fertility (Rf) gene in A2 hybrid system in pigeonpea (Cajanus cajan)

Inheritance of fertility restorer gene in pigeonpea was studied using F₂ and BC₁F₁ populations derived from cross AL103A × IC245273. It was found to be controlled by single dominant gene. Out of 228 SSR primer pairs, 33 primer pairs showed parental polymorphism, while four primers were found polymorphic in bulk segregant analysis (BSA). These four primers viz., CcM 1615, CcM 0710, CcM 0765 and CcM 1522 were used for genotyping of F₂ population and were found to be placed at 3.1, 5.1, 28.1 and 45.8 cM, respectively. Two of them, CcM 1615 and CcM 0710, evinced clear and unambiguous bands for fertility restoration in F₂ population. The Rf gene was mapped on linkage group 6 between the SSR markers CcM 1615 and CcM 0710 with the distances of 3.1 and 5.1 cM, respectively. The accuracy of the CcM 1615 was validated in 18 restorers and six maintainer lines. The marker CcM 1615 amplified in majority of male restorer lines with a selection accuracy of 91.66%.     

Molecular mapping of a new gene for resistance to frogeye leaf spot of soya bean in 'Peking'

Amplified fragment length polymorphism (AFLP) and microsatellite (simple sequence repeat, SSR) techniques were used to map the _RGSp_eking gene, which is resistant to most isolates of Cercospora sojina in the soya bean cultivar ‘Peking’. The mapping was conducted using a defined F₂ population derived from the cross of ‘Peking’(resistant) בLee’(susceptible). Of 64 EcoRI and MseI primer combinations, 30 produced polymorphisms between the two parents. The F₂ population, consisting of 116 individuals, was screened with the 30 AFLP primer pairs and three mapped SSR markers to detect markers possibly linked to Rcs_Peking. One AFLP marker amplified by primer pair E‐AAC/M‐CTA and one SSR marker Satt244 were identified to be linked to Res_Peking. The gene was located within a 2.1‐cM interval between markers AACCTA178 and Satt244, 1.1 cM from Satt244 and 1.0 cM from AACCTA178. Since the SSR markers Satt244 and Satt431 have been mapped to molecular linkage group (LG) J of soya bean, the Res_Peking resistance gene was putatively located on the LG J. This will provide soya bean breeders an opportunity to use these markers for marker‐assisted selection for frogeye leaf spot resistance in soya bean.     

Molecular mapping of black rot resistance locus Xca1bo on chromosome 3 in Indian cauliflower (Brassica oleracea var. botrytis L.)

Black rot is the most devastating disease of cauliflower worldwide causing severe damage to crop. The identification of markers linked to loci that control resistance can facilitate selection of plants for breeding programmes. In the present investigation, F₂ population derived from a cross between ‘Pusa Himjyoti’, a susceptible genotype, and ‘BR‐161’, a resistant genotype, was phenotyped by artificial inoculation using Xcc race 1. Segregation analysis of F₂ progeny indicated that a single dominant locus governed resistance to Xcc race 1 in ‘BR‐161’. Bulk segregant analysis in resistant and susceptible bulks of F₂ progeny revealed seven differentiating polymorphic markers (three RAPD, two ISSR and two SSR) of 102 markers screened. Subsequently, these markers were used to genotype the entire F₂ population, and a genetic linkage map covering 74.7 cM distance was developed. The major locus Xca1bo was mapped in 1.6‐cM interval flanked by the markers RAPD 04₈₃₃ and ISSR 11₆₃₅. The Xca1bo locus was located on chromosome 3. The linked markers will be useful for marker‐assisted resistance breeding in cauliflower.     

甜菜遗传连锁图谱初步构建

以甜菜高产低糖型JV34-2和低产高糖型2B023两材料杂交, 构建了200个单株的F₂作图群体, 利用所筛选出的56对SRAP引物组合和20对SSR引物, 对F₂作图群体进行PCR扩增和遗传连锁分析, 初步构建了一张包含9个连锁群、141个(123个SRAP和18个SSR)标记位点的甜菜遗传连锁图谱。该图谱覆盖长度为1399.88 cM, 平均图距9.92 cM。未进入连锁群的有4个标记。9个连锁群包含3~26个标记不等, 连锁群遗传距离15.69~237.21 cM。连锁群上有20.56%的标记出现偏分离, 主要集中在Ch3连锁群上, 其余分散在Ch1、Ch2、Ch8和Ch9中。该图谱是我国甜菜领域利用SRAP和SSR相结合方法, 构建的第一个较精密的分子遗传图谱, 为重要性状的基因定位和优良基因的克隆奠定了基础。