Molecular mapping of two recessive genes controlling resistance to bacterial leaf pustule disease in soybean (Glycine max)

Bacterial leaf pustule (BLP) caused by Xanthomonas axonopodis pv. glycines (Xag) is a serious soybean disease. A BLP resistant genotype ‘TS-3’ was crossed with a BLP susceptible genotype ‘PK472’, and a segregating F₂ mapping population was developed for genetic analysis and mapping. The F₂ population segregation pattern in 15:1 susceptible/resistance ratio against Xag inoculum indicated that the resistance to BLP in ‘TS-3’ was governed by two recessive genes. A total of 12 SSR markers, five SSR markers located on chromosome 2 and seven SSR markers located on chromosome 6 were identified as linked to BLP resistance. One of the resistance loci (r1) was mapped with flanking SSR markers Sat_183 and BARCSOYSSR_02_1613 at a distance of 0.9 and 2.1 cM, respectively. Similarly, SSR markers BARCSOYSSR_06_0024 and BARCSOYSSR_06_0013 flanked the second locus (r2) at distances of 1.5 and 2.1 cM, respectively. The identified two recessive genes imparting resistance to BLP disease and the SSR markers tightly linked to these loci would serve as important genetic and molecular resources to develop BLP resistant genotypes in soybean.     

Development of molecular markers linked to the <Emphasis Type="Italic">Fom-1</Emphasis> locus for resistance to Fusarium race 2 in melon

Fusarium wilt, caused by Fusarium oxysporum f. sp. melonis (F.o.m), is a worldwide soil-borne disease of melon (Cucumis melo L.). The most effective control measure available is the use of resistant varieties. Resistance to races 0 and 2 of this fungal pathogen is conditioned by the dominant gene Fom-1. An F₂ population derived from the ‘Charentais-Fom1’ × ‘TRG-1551’ cross was used in combination with bulked segregant analysis utilizing the random amplified polymorphic DNA (RAPD) markers, in order to develop molecular markers linked to the locus Fom-1. Four hundred decamer primers were screened to identify three RAPD markers (B17₆₄₉, V01₅₇₈, and V06₁₀₉₂) linked to Fom-1 locus. Fragments amplified by primers B17₆₄₉ and V01₅₇₈ were linked in coupling phase to Fom1, at 3.5 and 4 cM respectively, whereas V06₁₀₉₂ marker was linked in repulsion to the same dominant resistant allele at 15.1 cM from the Fom-1 locus. These RAPDs were cloned and sequenced in order to design primers that would amplify only the target fragment. The derived sequence characterized amplified region (SCAR) markers SB17₆₄₅ and SV01₅₇₄ (645 and 574 bp, respectively) were present only in the resistant parent. The SV06₁₀₉₂ marker amplified a band of 1092 bp only in the susceptible parent. These markers are more universal than the CAPS markers developed by Brotman et al. (Theor Appl Genet 10:337–345, 2005). The analysis of 24 melon accessions, representing several melon types, with these markers revealed that different melon types behaved differently with the developed markers supporting the theory of multiple, independent origins of resistance to races 0 and 2 of F.o.m.     

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.     

A novel blast resistance locus in a rice (<Emphasis Type="Italic">Oryza sativa</Emphasis> L.) cultivar,Chumroo, of Bhutan

The rice cultivar ‘Chumroo’ is commonly cultivated in the mid- and high-altitude areas of Bhutan. This cultivar has shown durable blast resistance in that area, without evidence of breakdown, for over 20 years. Chumroo was inoculated with 22 blast isolates selected from the race differential standard set of Japan. The cultivar showed resistance to all the isolates. To identify the resistance gene(s), Chumroo was crossed with a susceptible rice cultivar, Koshihikari. The F₁ plants of the cross showed resistance. Segregation analyses of 300 F₃ family lines fitted the segregation ratio of 1:2:1 and indicated that a single dominant gene controls the resistance to a blast isolate Ao 92-06-2 (race 337.1). The Chumroo resistance locus (termed Pi46(t)) was mapped between two SSR markers, RM6748 and RM5473, on the terminal region of the long arm of chromosome 4, using linkage analysis with SSR markers. The nearest marker, RM5473, was linked to the putative resistance locus at a map distance of 3.2 cM. At the chromosomal region, no true resistance genes were identified, whereas two field resistance genes were present. Therefore, we designated Pi46(t) as a novel blast resistance locus.     

Genetic control of resistance to Meloidogyne incognita race 1 in the Brazilian common bean (Phaseolus vulgaris L.) cv. Aporé

The use of resistant cultivars is one of the best methods for nematode control and reduction of economic losses caused by these pathogens. Studies of inheritance of nematode resistance in common bean (Phaseolus vulgaris L.) are nonetheless scarce. The present paper reports on the estimation of genetic parameters associated with resistance to the root nematode Meloidogyne incognita race 1 in common beans. Two contrasting bean lines, ‘Aporé’ (P₁ = nematode resistant) e ‘Macarr?o Rasteiro Conquista’ (P₂ = susceptible), and the generations F₁ (P₁ × P₂), F₂ (P₁ × P₂), BC₁(P₁) = (F₁ × P₁) and BC₁(P₂) = (F₁ × P₂), were assessed 45 days after nematode inoculation, through a scale related to the number of eggs per gram of root tissue. Dominant genetic effects were inferior in magnitude to additive effects, indicating incomplete dominance of nematode resistance. Dominance was in the direction of increased nematode resistance (i.e., lower number of eggs per g root). Resistance to Meloidogyne incognita race 1 in common bean is under control of a single gene locus, with incomplete dominance of the resistance allele present in ‘Aporé’, but modifier genes affecting its expression appear to be present in the susceptible parent ‘Macarr?o Rasteiro Conquista’.     

Identification and genetics of resistance to cercospora leaf spot (<Emphasis Type="Italic">Cercospora zonata</Emphasis>) in faba bean (<Emphasis Type="Italic">Vicia faba</Emphasis>)

The fungal disease cercospora leaf spot CLS (Cercospora zonata) has affected major faba bean (Vicia faba) production regions in southern Australian in the last several years. This study offers the first report of sources of resistance to CLS in faba bean and describes techniques to evaluate resistance to C. zonata in faba bean genotypes within a controlled environment. The method was rapid (43 days), repeatable (R ² > 0.74) and demonstrated positive correlations (R ² > 0.45–0.80) to data collected from field disease nurseries under naturally established CLS epiphytotics. All faba bean cultivars currently adopted by the Australian industry were found to be susceptible to CLS and defoliation was found to be an important component of disease expression. Genetic analysis of segregation patterns in F ₂ derived F ₃ families of 1322/2*Farah (resistant*susceptible) showed the mode of inheritance of resistance to C. zonata was monogenic dominant. F ₃ families were shown to segregate in the ratio of 1:2:1 for homozygous resistant: heterozygous: homozygous susceptible (χ₂² = 2.78; P > 0.05) and individual plants within heterozygous F ₃ families segregated in the ratio of 3:1 for resistant: susceptible responses (χ₁² = 2.93; P > 0.05). Monogenic dominant inheritance also explained the change in frequency of resistant and susceptible plants within a population of cv. Cairo following one generation of self-pollination (χ² = 0.88, 0.3 < P < 0.5). The sources of resistance identified in this study are being used to transfer CLS resistance to adapted faba bean genotypes for future cultivar releases to the southern Australian industry.     

Molecular mapping of a major QTL conferring resistance to SCMV based on immortal RIL population in maize

Sugarcane mosaic virus (SCMV) is one of devastating pathogens in maize (Zea mays L.), and causes serious yield loss in susceptible cultivars. An effective solution to control the virus is utilizing resistant genes to improve the resistance of susceptible materials, whereas the basic work is to analyze the genetic basis of resistance. In this study, maize inbred lines Huangzao4 (resistant) and Mo17 (susceptible) were used to establish an F₉ immortal recombinant inbred line (RIL) population containing 239 RILs. Based on this segregation population, a genetic map was constructed with 100 simple sequence repeat (SSR) markers selected from 370 markers, and it covers 1421.5 cM of genetic distance on ten chromosomes, with an average interval length of 14.2 cM. Analysis of the genetic map and resistance by mapping software indicated that a major quantitative trait locus (QTL) was between bin6.00 and bin6.01 on chromosome 6, linked with marker Bnlg1600 (0.1 cM of interval). This QTL could account for 50.0% of phenotypic variation, and could decrease 27.9% of disease index.     

Characterization of broad‐spectrum resistance to Soybean mosaic virus in soybean [Glycine max (L.) Merr.] cultivar ‘RN‐9’

Soybean mosaic virus (SMV) can cause serious yield losses in soybean. Soybean cultivar ‘RN‐9’ is resistant to 15 of 21 SMV strains. To well‐characterize this invaluable broad‐spectrum SMV‐resistance, populations (F₁, F₂ and F_2:3) derived from resistant (R) × susceptible (S) and R × R crosses were tested for SMV‐SC18 resistance. Genetic analysis revealed that SC18 resistance in ‘RN‐9’ plus two elite SMV‐resistant genotypes (‘Qihuang No.1’ and ‘Kefeng No.1’) are controlled by independently single dominant genes. Linkage analysis showed that the resistance of ‘RN‐9’ to SMV strains SC10, SC14, SC15 and SC18 is controlled by more than one gene(s). Moreover, Rsc10‐r and Rsc18‐r were both positioned between the two simple sequence repeats markers Satt286 and Satt277, while Rsc14‐r was fine‐mapped in 136.8‐kb genomic region containing sixteen genes, flanked by BARCSOYSSR_06_0786 and BARCSOYSSR_06_0790 at genetic distances of 3.79 and 4.14 cM, respectively. Allelic sequence comparison showed that Cytochrome P450‐encoding genes (Glyma.06g176000 and Glyma.06g176100) likely confer the resistance to SC14 in ‘RN‐9’. Our results would facilitate the breeding of broad‐spectrum and durable SMV resistance in soybeans.     

Genetics of angular leaf spot resistance in the Andean common bean accession G5686 and identification of markers linked to the resistance genes

Angular leaf spot (ALS), caused by the fungus Phaeoisariopsis griseola is an economically important and widely distributed disease of common bean. Due to the co-evolution of P. griseola with the large and small seeded bean gene pools, stacking Andean and Mesoamerican resistance genes is a strategy most likely to provide lasting resistance to ALS disease. This strategy requires identification and characterization of effective Andean and Mesoamerican resistance genes, and the development of molecular markers linked to these genes. This study was conducted to elucidate the genetics of ALS resistance in the Andean accession G5686 using an F₂ population derived from a G5686 × Sprite cross. Segregation analysis revealed that three dominant and complementary genes conditioned resistance of G5686 to P. griseola pathotype 31-0. Three microsatellite markers, Pv-ag004, Pv-at007 and Pv-ctt001 segregated in coupling phase with the resistance genes in G5686. Microsatellites Pv-ag004 and Pv-ctt001, located on opposite ends of linkage group B04 segregated with resistance genes Phg _G5686A , Phg _G5686B at 0.0 and 17.1 cM, respectively, while marker Pv-at007, localized on linkage group B09 segregated with resistance gene Phg _G5686C at 12.1 cM. Parental surveys showed that these markers were polymorphic in Andean and Mesoamerican backgrounds. The usefulness of G5686 ALS resistance genes in managing the ALS disease, and the potential utility of identified molecular markers for marker assisted breeding are discussed.     

Molecular mapping of a gene conferring resistance to Aphanomyces root rot (black root) in sugar beet (<Emphasis Type="Italic">Beta vulgaris</Emphasis> L.)

Caused by Aphanomyces cochlioides Drechsler, Aphanomyces root rot is a serious disease of sugar beet (Beta vulgaris L.), for which sources of resistance are scarce. To identify the segregation pattern of the rare resistance trait found in Japanese sugar beet line ‘NK-310mm-O’, F₁ and BC₁F₂ seedings, drawn from a cross between ‘NK-310mm-O’ and susceptible line ‘NK-184mm-O’, were inoculated with zoospores and their survival evaluated in the greenhouse. Resistance segregation followed was that of a single dominant gene, which was designated Acr1 (Aphanomyces cochlioides resistance 1). Molecular markers tightly linked to Acr1 were identified by bulked segregant analysis of two BC₁F₂ populations. Fourteen AFLP markers linked to Acr1 were identified, the closest located within ±3.3 cM. Three F₅ lines and two BC₂F₁ lines, selected on the basis of their Acr1-AFLP markers, were tested for their resistance to Aphanomyces root rot in a highly infested field. Results indicated that Acr1 conferred significant resistance to Aphanomyces root rot at the field level. Based on its linkage with CAPS marker tk, a representative marker for chromosome III, Acr1 was located on this chromosome. The clear linkage between tk and Rhizomania resistance trait Rz1, suggests the clustering of major disease resistance genes on chromosome III.     

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.     

Molecular mapping of <Emphasis Type="Italic">Pc68</Emphasis>, a crown rust resistance gene in <Emphasis Type="Italic">Avena</Emphasis><Emphasis Type="Italic">sativa</Emphasis>

Crown rust, which is caused by Puccinia coronata f. sp. avenae, P. Syd. & Syd., is the most destructive disease of cultivated oats (Avena sativa L.) throughout the world. Resistance to the disease that is based on a single gene is often short-lived because of the extremely great genetic diversity of P. coronata, which suggests that there is a need to develop oat cultivars with several resistance genes. This study aimed to identify amplified fragment length polymorphism AFLP markers that are linked to the major resistance gene, Pc68, and to amplify the F₆ genetic map from Pc68/5*Starter × UFRGS8. Seventy-eight markers with normal segregation were discovered and distributed in 12 linkage groups. The map covered 409.4 cM of the Avena sativa genome. Two AFLP markers were linked in repulsion to Pc68: U8PM22 and U8PM25, which flank the gene at 18.60 and 18.83 centiMorgans (cM), respectively. The marker U8PM25 is located in the linkage group 4_12 in the Kanota × Ogle reference oat population. These markers should be useful for transferring Pc68 to genotypes with good agronomic characteristics and for pyramiding crown rust resistance genes.     

Identification of DNA markers linked to an induced mutated gene conferring resistance to powdery mildew in pea (<Emphasis Type="Italic">Pisum sativum</Emphasis> L.)

We have recently induced two powdery mildew (Erysiphe pisi Syd) resistant mutants in Pisum sativum L. via ethylnitrosourea (ENU) mutagenesis. Both mutations (er1mut1 and er1mut2) affected the same locus er1 that determines most of the identified natural sources of powdery mildew resistance (PMR) in this crop. The mutated gene er1mut2 was mapped to a linkage group of 16 DNA markers combining three main strategies: near isogenic lines (NILs) analysis, bulked segregant analysis and genetic mapping of randomly identified polymorphic markers, together with three DNA-markers techniques: ISSR, RAPDs and AFLPs. Markers located closer to the PMR locus, OPO06_1100y (0.5 cM), OPT06₄₈₀ (3.3 cM) and AGG/CAA₁₂₅ (5.5 cM), were cloned and converted into SCAR markers. Markers AH1R₈₅₀ and AHR_920y were found to be allelic and converted into the co-dominant marker ScAH1 (16.3 cM). Two previously known DNA markers, ScOPE16₁₆₀₀ and A5_420y, were mapped at 9.6 and 23.0 cM from the PMR locus, respectively. The novel markers identified in this study are currently being transferred to a new F2 mapping population derived from a cross between the induced PMR mutant line F(er1mut2) and a more genetically distant susceptible line of Pisum sativum var. arvense.     

Mapping of a novel,major late blight resistance locus in the diploid (1EBN) Mexican Solanum pinnatisectum Dunal on chromosome VII

Late blight caused by the oomycete Phytophthora infestans (Mont.) de Bary (Pi) is the most important foliar disease of potato worldwide. An intraspecific hybrid between individuals of a resistant and a susceptible S. pinnatisectum accession was backcrossed to the susceptible parent to generate a segregating population for late blight resistance consisting of 84 plants. In detached‐leaflet assays, reaction to late blight segregated in a 1r:1s manner in BC₁ progeny indicating the presence of a single dominant resistance gene. A genetic map was constructed based on 1,583 DArT/SSR markers which were allocated to 12 linkage groups, covering 1,793.5 cM with an average marker distance of 1.1 cM. The late blight resistance locus derived from S. pinnatisectum was mapped on chromosome VII. In comparison with the previously reported resistance genes Rpi1 and Rpi2, the new target resistance locus most likely is located on the opposite arm of chromosome VII. Results of this study will serve as a basis for future fine mapping of the late blight resistance locus and the development of locus‐specific markers for marker‐assisted selection.     

Identification and characterization of RAPD and SCAR markers linked to anthracnose resistance gene in sorghum [Sorghum bicolor (L.) Moench]

Anthracnose, one of the destructive foliar diseases of sorghum growing in warm humid regions, is incited by the fungus Colletotrichum graminicola.The inheritance of anthracnose resistance was studied using the parental cultivars of Sorghum bicolor (L.) Moench, HC 136 (susceptible to anthracnose) and G 73 (anthracnose resistant). The F₁ and F₂ plants were inoculated with the local isolates of C. graminicola cultures. The F₂ plants showed a segregation ratio of 3 (susceptible): 1(resistant) indicating that the locus for resistance to anthracnose in sorghum accession G 73 segregates as a recessive trait in a cross to susceptible cultivar HC 136. RAPD (random amplified polymorphic DNA) marker OPJ 01₁₄₃₇ was identified as marker closely linked to anthracnose resistance gene in sorghum by bulked segregant analysis of HC 136 × G73 derived recombinant inbred lines (RILs) of sorghum. A total of 84 random decamer primers were used to screen polymorphism among the parental genotypes. Among these, only 24 primers were polymorphic. On bulked segregant analysis, primer OPJ 01 amplified a 1437 bp fragment only in resistant parent G 73 and resistant bulk. The marker OPJ 01₁₄₃₇ was cloned and sequenced. The sequence of RAPD marker OPJ 01₁₄₃₇ was used to generate specific markers called sequence characterized amplified regions (SCARs). A pair of SCAR markers SCJ 01-1 and SCJ 01-2 was developed using Mac Vector program. SCAR amplification of resistant and susceptible parents along with their respective bulks and RILs confirmed that SCAR marker SCJ 01 is at the same loci as that of RAPD marker OPJ 01₁₄₃₇ and hence, is linked to anthracnose resistance gene. Resistant parent G 73 and resistant bulk amplified single specific band on PCR amplification using SCAR primer pairs. The RAPD marker OPJ 01₁₄₃₇ was mapped at a distance of 3.26 cM apart from the locus governing anthracnose resistance on the sorghum genetic map by the segregation analysis of the RILs. Using BLAST program, it was found that the marker showed 100 per cent alignment with the contig{_}3966 located on the longer arm of chromosome 8 of sorghum genome. Therefore, these identified RAPD and SCAR markers can be used in the resistance-breeding program of sorghum anthracnose by marker-assisted selection.An erratum to this article can be found at     

User‐friendly markers linked to Fusarium wilt race 1 resistance Fw gene for marker‐assisted selection in pea

Fusarium wilt is one of the most widespread diseases of pea. Resistance to Fusarium wilt race 1 was reported as a single gene, Fw, located on linkage group III. The previously reported AFLP and RAPD markers linked to Fw have limited usage in marker‐assisted selection due to their map distance and linkage phase. Using 80 F₈ recombinant inbred lines (RILs) derived from the cross of Green Arrow × PI 179449, we amplified 72 polymorphic markers between resistant and susceptible lines with the target region amplified polymorphism (TRAP) technique. Marker–trait association analysis revealed a significant association. Five candidate markers were identified and three were converted into user‐friendly dominant SCAR markers. Forty‐eight pea cultivars with known resistant or susceptible phenotypes to Fusarium wilt race 1 verified the marker–trait association. These three markers, Fw_Trap_480, Fw_Trap_340 and Fw_Trap_220, are tightly linked to and only 1.2 cM away from the Fw locus and are therefore ideal for marker‐assisted selection. These newly identified markers are useful to assist in the isolation of the Fusarium wilt race 1 resistance gene in pea.     

Genetic analysis of resistance to <Emphasis Type="Italic">Fusarium</Emphasis> root rot in common bean

Fusarium root rot (FRR) is a major disease of common bean worldwide. Knowledge of the inheritance of resistance to FRR would be important in devising strategies to breed resistant varieties. Therefore, a 12 × 12 full diallel mating scheme with reciprocal crosses was performed to generate 132 F₁ progenies, which were then advanced to the F₃. The progenies were evaluated for resistance to FRR under green house conditions in Uganda. General combining ability (GCA) effects were highly significant (P ≤ 0.01) for disease scores. Specific combining ability effects were not significant (P > 0.05) in the F₁, but were highly significant (P < 0.01) in the F₃ generation. These results indicate that resistance to FRR was governed by genes with additive effects in combination with genes with non-additive effects. Reciprocal differences were also significant (P = 0.01) at F₁ and F₃, primarily reflecting a large influence of maternal effects in both these generations. In fact, susceptible parents did not differ significantly (P > 0.05) for disease scores when used as paternal parents in the F₃, but differed strongly as maternal parents (P = 0.0002). Generally, the progenies were distinctly more resistant when the resistant parent was used as the female in crosses, especially as observed in the F₃. The maternal effects were strong in the F₃ generation, suggesting a complex form of cytoplasmic–genetic interaction. The non-maternal reciprocal effects in the F₃ were significant (P < 0.05) in both the resistant × resistant diallel, and in the resistant × susceptible crosses. Mid-parent heterosis (MPH) occurred in most crosses, with average heterosis approximately equal in each of the three generations, indicating that epistasis was probably more influential than dominance of individual genes. Gene-number formulas indicated that several genes were involved in resistant × susceptible crosses. Among resistant × resistant crosses, many produced continuous distributions of F₁ progeny scores, suggesting polygenic inheritance, while bi-modal distributions were characteristic of the F₃ distributions, and fit expected ratios for two or three loci segregating in each cross. Dominant forms of epistasis favoring resistance were strongly indicated. Parent–offspring heritability estimates were moderate. Overall, the results indicate that resistant parents contain a number of different resistance genes that can be combined with the expectation of producing strong and durable resistance. The lines MLB-49-89A, MLB-48-89, RWR719 and Vuninkingi, with large and negative GCA effects, contributed high levels of resistance in crosses and would be recommended for use in breeding programs.     

Identification of molecular markers associated with resistance to squash silverleaf disorder in summer squash (<Emphasis Type="Italic">Cucurbita</Emphasis> <Emphasis Type="Italic">pepo</Emphasis>)

Squash silverleaf (SSL), caused by the silverleaf whitefly [Bemisia argentifolii (formerly known as Bemisia tabaci Gennadius, B strain)], is an important physiological disorder that affects squash (Cucurbita spp.) by reducing yield potential. Breeding squash with resistance to SSL disorder can be facilitated by using marker-assisted selection (MAS). Resistance to SSL disorder, in Cucurbita pepo, is conferred by a single recessive gene (sl). The objective of this study was to identify molecular markers associated with resistance. A zucchini squash, SSL disorder resistant breeding line, ‘Zuc76’ (sl/sl) and a SSL disorder susceptible zucchini cultivar ‘Black Beauty’ (Sl/Sl) were screened with 1,152 randomly amplified polymorphic DNA (RAPD) primers and 432 simple sequence repeat (SSR) markers to identify polymorphisms. Using F₂ and BC₁ progeny segregating for SSL disorder resistance, three RAPD (OPC07, OPL07 and OPBC16) primers and one SSR (M121) marker were found associated with sl. Fragments amplified by RAPD primer OPC07 was linked in coupling phase to sl, whereas RAPD primer OPL07 was linked in repulsion phase. RAPD primer OPBC16 and SSR marker M121 were co-dominant. The allelic order of these loci was found to be M121–sl–OPC07–OPL07–OPBC16. The closest marker to sl is M121 with an estimated genetic distance of 3.3 cM. The markers identified in this study will be useful for breeding summer squash (C. pepo) for SSL disorder resistance derived from zucchini squash breeding line ‘Zuc76’.     

青海大黄油菜粒色性状分子标记的开发和图谱整合

利用青海大黄油菜和褐籽白菜型油菜09A-126构建BC₄和F₂分离群体, 结合AFLP与群体分离分析法(bulked segregant analysis, BSA)筛选引物, 获得5个与黄籽基因Brsc1紧密连锁的分子标记Y11~Y15。5个AFLP特异片段的序列, 均与白菜型油菜的A9染色体部分序列表现同源。将5个AFLP标记成功转化为5个SCAR标记(SC11~SC15)。利用目标基因所在染色体区段序列筛选到7个与目标基因紧密连锁的SSR标记(BrID10607、KS10760、B089L03-3和A1~A4)。利用SCAR和SSR标记扫描F₂群体中部分单株, 发现SC14和A1为共显性标记。用BC₄群体将Brsc1定位在标记Y06和A4之间1.7 Mb的区间内, 遗传距离分别为0.115 cM和0.98 cM。标记Y05和Y12与Brsc1共分离。本研究为黄籽油菜分子标记辅助选择育种体系的建立及目标基因的进一步精细定位和图位克隆奠定了基础。     

Mapping and confirmation of two genes conferring resistance to soybean rust (Phakopsora pachyrhizi) in the soybean line UG-5 (Glycine max)

Development of durable resistance to soybean rust (SBR) is challenging due to the pathogenic diversity of Phakopsora pachyrhizi populations. The objective of this research was to investigate and confirm the genomic locations of Rpp genes in the Ugandan line UG-5 that confer resistance to different SBR pathotypes. Bulked segregant analysis revealed two genomic regions associated with resistance in a cross with rust-susceptible 'Williams 82'. Composite interval mapping in the F₂ and F_2:3 populations had a LOD score of 48.7 in a region 0.38 cM away from the estimated location of the Rpp1 locus on chromosome (Chr.) 18. An approximately 23-Kbp interval spanning the Rpp1 locus was flanked by SNP markers ss715632313 and ss715632318. Another interval was identified at the Rpp3 locus on Chr. 6 between markers Satt100 and ss715594488 (2.4 cM) in the F₂ population and between Satt100 and ss715594874 (4.3 cM) in the F_2:3 population, with a maximum LOD score of 25.6. UG-5 was thus confirmed to have SBR resistance genes at the Rpp1 and Rpp3 loci that can be pyramided into other elite cultivars.