Resistance profile of improved cassava germplasm to cassava mosaic disease in Nigeria

Cassava mosaic disease (CMD) caused by a group of begomoviruses and transmitted by whitefly vector is a serious disease in all the cassava-growing areas of Africa. Field evaluation with replication was conducted in 2003 and 2004 in three agroecologies in Nigeria to study the response of 40 cassava genotypes to CMD and to investigate genotype × environment (GE) interactions on their reactions to CMD, using the rank-sum classification and site regression analysis model. The 40 genotypes were separated into resistant (n = 17), moderately resistant (n = 6), moderately susceptible (n = 2) and susceptible (n = 15) groups. Environments, genotypes and GE interactions were all highly significant (P < 0.0001) for the virus disease contributing 9.5%, 71.36% and 19.14%, respectively to total variation. More than 40% of the genotypes were identified as resistant to the disease. Genotypes TMS 98/0581, TMS 99/3073, TMS 97/4763, TMS M98/0040, TMS 98/0505, TMS 97/0211, TMS 97/4769, TMS 99/2123, TMS M98/0068 and TMS 97/0162 were shown to have high resistance to CMD. The study also identified Umudike, in south-east Nigeria, as having high disease severity and the most appropriate site for CMD resistance screening of genotypes. Most of the genotypes exhibited stable resistance to CMD. The implication that the availability of these resistant genotypes as identified in this study could be a source of CMD resistance for further breeding is discussed.     

Assessment of sweet cherry (<Emphasis Type="Italic">Prunus avium</Emphasis> L.) genotypes for response to bacterial canker disease

Integration of alleles for bacterial canker resistance into new sweet cherry cultivars requires information on the sources of resistance in the germplasm. Five market-leading sweet cherry cultivars, ‘Rainier’, ‘Sweetheart’, ‘Bing’, ‘Regina’ and ‘Chelan’, advanced selections ‘AA’, ‘BB’, ‘CC’, ‘DD’, ‘EE’, ‘GG’, and ‘PMR-1’ used as breeding parents in the Washington State University’s Sweet Cherry Breeding Program were evaluated. Comparative genotypic disease severity was obtained with three methods of inoculation (leaf wounding with carborundum, cut wounds in leaf mid-rib and shoot tip) on whole plants. Additionally, genotypic data on susceptibility of detached leaves versus fruit and an assessment of the movement of Pseudomonas syringae pv. syringae (Pss) population in inoculated shoots were obtained. Genotype susceptibility was significantly (P ≤ 0.05) influenced by inoculation method, with shoot inoculation providing the best separation of resistance levels among genotypes. A low correlation (r = 0.26, P = 0.21) was observed between disease responses measured on detached leaf versus fruit, while a moderately high correlation (r = 0.50, P = 0.10) was found among bacterial populations in the tissues and in the degree of symptoms expressed. By all comparative methods, the advanced selections, as well as, ‘PMR-1’, were less susceptible than the market-leading cultivars. Also, movement of Pss from shoot tip inoculation points to the shoot base was not detected for advanced selections ‘AA’, ‘BB’, ‘DD’, and ‘EE’. This study reveals that the advanced selections could be potential sources of resistance alleles to bacterial canker. This is the first evaluation of the advanced selections for bacterial canker disease.     

Number of involved genes and heritability of clover rot (Sclerotinia trifoliorum) resistance in red clover (Trifolium pratense)

European red clover (Trifolium pratense) crops are challenged by clover rot, a devastating disease caused by Sclerotinia trifoliorum or, in some cases by S. sclerotiorum. No completely resistant cultivars are available and resistance breeding is hampered by the lack of knowledge on the number of involved resistance genes and the heritability of clover rot resistance. In this study, we estimated the number of major genes contributing to clover rot resistance by analysing 15 F₁ progeny populations from pair crosses between ramets of resistant and susceptible genotypes. Parent plants were chosen from diverse, diploid populations, including wild material, landraces and cultivars. Young progeny plants were inoculated with ascospores, evaluated phenotypically and the segregation of disease scores was studied. Our results indicated that clover rot resistance may be conferred by three major effect genes, although segregation patterns suggested that there may be numerous minor effect genes involved as well. No proof was found for a maternal inheritance of clover rot resistance. To get insight in the heritability of clover rot resistance, we applied divergent selection by our high-throughput bio-test on an experimental diploid population: the original population (70.5 %), the first generation after selection for susceptibility (79.2 %) and the first generation after selection for resistance (62.3 %) differed significantly in susceptibility (p < 0.001). The second generation after selection for resistance (60.0 %) was not more resistant than the first generation after selection for resistance. In the first generation of selection the heritability (h²) was on average 0.34. In the second generation of selection h² was 0.07. These findings have important implications for resistance breeding.     

Evaluation of Verticillium wilt resistance in commercial cultivars and advanced breeding lines of cotton

Verticillium wilt (VW), caused by Verticillium dahliae Kleb, is one of the most destructive diseases in cotton (Gossypium spp.). The most efficient and cost-effective method of controlling the disease is the use of resistant cotton cultivars. Most commercial cultivars and elite breeding lines are developed under non-VW conditions and their responses to the disease are currently unknown. This study was conducted to evaluate current commercial cotton cultivars and advanced breeding lines for VW resistance. In 2011–2013, a total of 84 cultivars from major US seed companies, 52 advanced breeding lines from the US public breeding programs, and 87 introgression lines from a cross between Acala 1517-99 × Pima PHY 76 from the New Mexico Cotton Breeding Program, were evaluated for VW resistance in the greenhouse. Cotton cultivars and breeding lines were evaluated in ten separate replicated tests by inoculation with a defoliating-type isolate of V. dahliae. While leaf severity rating and percentages of infected plants, infected leaves and defoliated leaves were found to be significantly and positively correlated with one another, leaf severity rating and percentage of infected leaves were best choices because of their relatively low coefficients of variation and higher resolutions to differentiate resistant genotypes from susceptible ones. The heritabilities for the VW resistance traits ranged from 0.58 to 0.80 with an average of 0.67, indicating that variation in VW resistance is predominantly due to genetic factors. Of the 223 commercial cultivars and advanced lines, six Upland cultivars (FM 9160B2F, FM 9170 B2F, NG 4010 B2RF, Nitro 44 B2RF, DP 1219 B2RF, and ST 4288 B2F), five advanced lines (Ark 0403-3, MD 10-5, MD 25ne, NC11AZ01, and PD 0504), two introgression lines from Upland × Pima (NM11Q1157 and 08N1618), and four Pima cultivars (COBALT, DP 357, PHY 800, and PHY 830) had higher levels of resistance to VW. The resistance shown by most of these cultivars in the greenhouse was consistent with their performance in previous field tests. Based on the initial VW resistance, 19 highly or moderately resistant genotypes were chosen for re-evaluation and 30 genotypes were also assessed more than once for VW resistance in different tests, most of which had concordant performance. These cultivars and advanced lines should be useful resources to improve VW resistance in cotton breeding.     

Sources of resistance to Fusarium head blight in VIR oat collection

Fusarium head blight (FBH) is a serious disease of cultivated oats (Avena sativa L.). The objective of this study was to screen a set of oat genotypes from the VIR Avena sativa germplasm collection for the FHB resistance. Of the 155 screened genotypes 42 % belonged to both hulled and naked cultivars, 55 % were landraces and the rest were breeding lines. Screening nurseries were planted at two locations: in the Northwestern Russia in 2007–2008 with artificial inoculation by F. sporotrichioides strains and in the Russian Far East in 2009 (natural infections). The resistance data were based on three different parameters: (a) percentage of grain showing evidence of Fusarium damage, (b) the DNA content of the trichothecene-producing Fusarium species and (c) the trichothecene mycotoxin accumulation; the sum of which permitted identification of genotypes with multicomponent resistance to FHB. The highest degrees of resistance were observed in the naked cvs. Iymay (k-11014, China) and Numbat (k-14851, Australia) and by the hulled cv. Kuromi (к-11632, Japan). The most resistant landraces were the hulled oats originating from the Asian region (k-2513, k-6963, k-7766, and k-8479). Considerable similarity was observed between the resistance reactions of oat genotypes to the Fusarium disease under different environmental conditions. The identified resistant accessions may serve as crossing partners in oat breeding efforts.     

Genetic and histological characterization of downy mildew resistance at the cotyledon stage in <Emphasis Type="Italic">Raphanus sativus</Emphasis> L.

Downy mildew (DM; Hyaloperonospora brassicae) is one of the most serious diseases in radish and responsible for high production losses. The objectives of this study were (1) to identify new sources of DM resistance at the cotyledon stage; (2) to determine the inheritance of the resistance; and (3) to clarify the histological and cellular response involved in DM infection. We screened 200 radish accessions for DM resistance at the cotyledon stage. Radish accessions Rd001, Rd004, Rd048 and Rd150 showed a complete resistance response (hypersensitive reaction), and accession Rd193 exhibited a partial resistance with confined sporulation. The highly susceptible accession Rd197 was then crossed with all resistant genotypes for a genetic analysis. F₂ segregation analysis suggested that cotyledon resistance in Rd001, Rd004, Rd048 and Rd150 is conferred by a single dominant gene while resistance in Rd193 is polygenic. Genetic data suggests Rd193 resistance might be conferred by two dominant genes with complementary action, althought further experiments are needed to confirm this hypothesis. To conduct a histological study using light and fluorescence microscopy, we collected cotyledons from three genotypes with either differing levels of resistance (Rd004 and Rd193) and high susceptibility (Rd197) at ten different time points, from 3 h to 7 days post inoculation. Tissue necrosis was responsible for the inhibition and reduction of H. brassicae growth in Rd004 and Rd193 within 24 h of inoculation. For susceptible accession Rd197, the first evidence of necrotic cells appeared 48 h post inoculation. Callose deposition associated with intercellular H. brassicae growth occurred 3 h post inoculation for all genotypes and was the lowest in resistant accession Rd004. Cotyledon resistance to DM identified in radish is of high commercial interest and has the potential to be used in breeding programs.     

Identification of markers associated with bacterial blight resistance loci in cowpea [Vigna unguiculata (L.) Walp.]

Cowpea bacterial blight (CoBB), caused by Xanthomonas axonopodis pv. vignicola (Xav), is a worldwide major disease of cowpea [Vigna unguiculata (L.) Walp.]. Among different strategies to control the disease including cultural practices, intercropping, application of chemicals, and sowing pathogen-free seeds, planting of cowpea genotypes with resistance to the pathogen would be the most attractive option to the resource poor cowpea farmers in sub-Saharan Africa. Breeding resistance cultivars would be facilitated by marker-assisted selection (MAS). In order to identify loci with effects on resistance to this pathogen and map QTLs controlling resistance to CoBB, eleven cowpea genotypes were screened for resistance to bacterial blight using 2 virulent Xav18 and Xav19 strains isolated from Kano (Nigeria). Two cowpea genotypes Danila and Tvu7778 were identified to contrast in their responses to foliar disease expression following leaf infection with pathogen. A set of recombinant inbred lines (RILs) comprising 113 individuals derived from Danila (resistant parent) and Tvu7778 (susceptible parent) were infected with CoBB using leaf inoculation method. The experiments were conducted under greenhouse conditions (2007 and 2008) and disease severity was visually assessed using a scale where 0 = no disease and 4 = maximum susceptibility with leaf drop. A single nucleotide polymorphism (SNP) genetic map with 282 SNP markers constructed from the same RIL population was used to perform QTL analysis. Using Kruskall-Wallis and Multiple-QTL model of MapQTL 5, three QTLs, CoBB-1, CoBB-2 and CoBB-3 were identified on linkage group LG3, LG5 and LG9 respectively showing that potential resistance candidate genes cosegregated with CoBB resistance phenotypes. Two of the QTLs CoBB-1, CoBB-2 were consistently confirmed in the two experiments accounting for up to 22.1 and to 17.4% respectively for the first and second experiments. Whereas CoBB-3 was only discovered for the first experiment (2007) with less phenotypic variation explained of about 10%. Our results represent a resource for molecular marker development that can be used for marker assisted selection of bacterial blight resistance in cowpea.     

Mapping association of molecular markers and sheath blight (<Emphasis Type="Italic">Rhizoctonia solani</Emphasis>) disease resistance and identification of novel resistance sources and loci in rice

Sheath blight (ShB) disease caused by Rhizoctonia solani is one of the major threats to rice crop world-wide. Progress in breeding for resistant rice varieties is limited due to lack of highly resistant germplasm against sheath blight. In present study, diverse rice landrace were phenotyped against R. solani and resistant and moderately resistant sources were identified from the panel of 134 germplasm pool. Landrace Nizam shait showed resistance, where as Bidar local-2, Jigguvaratiga, NavaliSali, Jaddu and Tetep exhibited moderate resistance. Population structure was analysed by genotyping the accessions using 63 genome wide Rice Microsatellite markers which divided the mapping panel into two groups. Association mapping using GLM?+?Q model of TASSEL indicated significant association between twenty-one marker loci on nine chromosomes with ShB resistance with phenotypic variation (R²) ranging 3.02–22.71 per cent. We identified 13 new markers to be associated with ShB resistance. The present work validates previously identified eight markers flanking different shB QTLs. None of the allele from the tested markers was unique and common among resistant and moderately resistant landraces identified in this work except allele 420 bp of RM337 and allele 310 bp of RM5556 noticed only in Tetep. Our findings predict the possible presence of unreported QTL region in marker interval of RM337 and RM5556 on chromosome 8 for ShB resistance in Tetep which invites further investigation.     

Bru1 gene and potential alternative sources of resistance to sugarcane brown rust disease

Brown rust, caused by the fungus Puccinia melanocephala, is responsible for important yield losses in sugarcane production globally and it is therefore an important objective to introduce resistance to this disease in breeding programs. A major gene, Bru1, has been shown to confer resistance to P. melanocephala strains from different parts of the world and two molecular markers, R12H16 and 9O20-F4, closely associated to this gene have been previously reported. The usefulness of these molecular diagnostic markers in order to predict a rust resistant phenotype under natural high pressure inoculums conditions was analyzed. A total of 129 sugarcane accessions were evaluated under field infection for resistance or susceptibility to brown rust and subsequently screened for presence or absence of the two Bru1 diagnostic markers. A total of 49 genotypes (38 %) were phenotyped as resistant to brown rust but only eight (16.3 %) of them were harboring the Bru1 gene. To determine overall frequency of the Bru1 in the local sugarcane germplasm collection, 190 additional genotypes were examined. Presence of Bru1, as determined by the diagnostic markers, was detected in only 7 % of the genotypes evaluated. In conclusion, Bru1 diagnostic markers enable positive selection for brown rust resistance in sugarcane and moreover allowed detecting at least one additional source(s) of resistance. Interestingly, whilst only little genetic variability of rust resistance independent of Bru1 has been reported previously, this alternative genetic resource(s) found in our local germplasm constitutes the predominant one and should be helpful in order to amplify the narrow genetic basis for brown rust resistance in sugarcane.     

Quantitative trait locus mapping for Verticillium wilt resistance in a backcross inbred line population of cotton (Gossypium hirsutum × Gossypium barbadense) based on RGA-AFLP analysis

Verticillium wilt (VW), caused by Verticillium dahliae Kleb., is one of the most important diseases in cotton. The objective of this study was to map quantitative trait loci (QTLs) conferring VW resistance using resistance gene analog (RGA)-targeted amplified fragment length polymorphism (RGA-AFLP) markers in an interspecific backcross inbred line mapping population, consisting of 146 lines from a susceptible Sure-Grow 747 (Gossypium hirsutum L.) × resistant Pima S-7 (G. barbadense L.) cross. VW resistance was evaluated in replicated tests based on disease incidence in the field, and disease incidence and severity in the greenhouse. Of 160 polymorphic RGA-AFLP markers, 42 were significantly correlated with one or more VW traits and 41 were placed on a linkage map which covered 1,226 cM of the cotton genome and contained 251 other molecular markers. Three QTLs for VW resistance were detected, each of which explained 12.0–18.6 % of the phenotypic variation. Two of these QTLs for disease incidence and severity detected in the greenhouse inoculation tests using root wounding are located on chromosome c4. Both are closely linked to four RGA-AFLP markers and therefore considered as the same QTL for VW resistance. The other QTL detected in the field test was located on c19 and flanked by several RGA-AFLP markers. The desirable QTL allele on c4 for VW resistance detected in the greenhouse was from the VW susceptible Upland parent and absent from the resistant Pima parent which was more VW susceptible due to the disarmament of the first line of defense mechanism due to root wounding during inoculation. The other desirable VW resistance QTL allele, on c19, was from the resistant parent Pima S-7, consistent with the fact that Pima cotton was more resistant to VW when naturally infected in the field. The results should facilitate the development of more sequence specific markers and the transfer of VW resistance from Pima to Upland cotton through marker-assisted selection.     

Genotypic variation of resistance to southern stem rot of Jerusalem artichoke caused by Sclerotium rolfsii

Southern stem rot caused by Sclerotium rolfsii is a significant problem of Jerusalem artichoke (Helianthus tuberosus L.) production in Thailand. Resistant varieties are not available. The objective of this study was to investigate genetic variability of Jerusalem artichoke genotypes for resistance to stem rot caused by S. rolfsii. Ninety-one Jerusalem artichoke genotypes were evaluated under greenhouse conditions. Traits evaluated included disease score, lesion length, days to permanent wilting, plant height, shoot dry weight, and root dry weight index. Number of days from inoculation until permanent wilting was the only trait with statistically significant differences among genotypes. Based on this trait, genotypes were categorized into two distinct groups: resistant and susceptible. Genotypes that consistently expressed relative resistance to S. rolfsii included HEL 280, HEL 278, HEL 293 and JA 98. These genotypes may be useful to plant breeders as sources of germplasm for incorporating resistance to S. rolfsii into Jerusalem artichoke.     

Inheritance of resistance to Fusarium oxysporum f. sp. cubense race 1 in bananas

Fusarium wilt of bananas (also known as Panama disease), caused by the soil-borne fungus Fusarium oxysporum f. sp cubense (Foc), is a serious problem to banana production worldwide. Genetic resistance offers the most promising means to the control of Fusarium wilt of bananas. In this study, the inheritance of resistance in Musa to Foc race 1 was investigated in three F₂ populations derived from a cross between ‘Sukali Ndizi’ and ‘TMB2X8075-7’. A total of 163 F₂ progenies were evaluated for their response to Fusarium wilt in a screen house experiment. One hundred and fifteen progenies were susceptible and 48 were resistant. Mendelian segregation analysis for susceptible versus resistant progenies fits the segregation ratio of 3:1 (χ² = 1.72, P = 0.81), suggesting that resistance to Fusarium wilt in Musa is conditioned by a single recessive gene. We propose panama disease 1 to be the name of the recessive gene conditioning resistance to Fusarium wilt in the diploid banana ‘TMB2X8075-7’.     

Marker assisted backcrossing for introgression of Fusarium wilt resistance gene into melon

Fusarium wilt, caused by Fusarium oxysporum f. sp. melonis is a common vascular wilt fungal disease in melon across the world. The resistance gene to race 1 of this causal agent, Fom-2, has been previously cloned and its sequence is available. The objective of this research was the introgression of Fom-2 from one resistant (Isabelle) genotype into two susceptible cultivars (Garmak and Tile-torogh) via marker assisted backcrossing. First, the leucine-rich repeats (LRR) domain of Fom-2 from resistant and susceptible genotypes was sequenced to develop functional markers. A length of 1274 bp of the 3′ end of this gene was isolated, cloned and sequenced. The difference between resistant and susceptible genotypes in this region was 28 nucleotide substitutions. Two allele specific primer pairs, Fom2-R409 and Fom2-S253, were designed based on nucleotide substitutions to amplify resistant and susceptible alleles, respectively. For introgression of the gene, donor (Isabelle) and recurrent (Garmak and Tile-torogh) parents were crossed. Resistant plants in BC₁F₁ and BC₂F₁ generations were first detected using artificial pathogen inoculation and later the plants were genotyped by functional markers to validate their resistance. The resistant plants were also selected phenotypically in each generation for background genome recovery, which conduced to high similarity of BC₃ generation with the recurrent parents. It was proved the developed markers are more precise and efficient than inoculation trial and could be used as confident tools for screening of resistant melon genotypes to Fusarium wilt.     

Selection of cassava accessions with multiple resistance to pathogens associated with root rot disease

Cassava root rot disease (CRRD) severely affects productivity in several countries. The objective of this study was to estimate genetic parameters and to identify multiple resistance sources against pathogens associated with CRRD. The symptoms caused by Fusarium spp., Phytophthora spp., and Botryosphaeriaceae species in peel and pulp from the roots were evaluated in 277 accessions using a whole tuberous root inoculation method. The resistance data were obtained by REML/BLUP (restricted maximum likelihood/best linear unbiased predictor). The classic selection index (CI), multiplicative (MI), and sum of ranks (SRI) were used to identify the accessions with multiple resistance. For all pathogens, the environmental variance (\(\sigma_{e}^{2}\)) was the most important component. Individual heritability \(\left( {h_{g}^{2} } \right)\) was of low magnitude for resistance to most pathogens (0.16 ± 0.02—peel and 0.31 ± 0.03—pulp for Fusarium spp.; 0.26 ± 0.03—peel and 0.30 ± 0.03—pulp for Phytophthora spp.; and 0.28 ± 0.03—peel and 0.27 ± 0.03—pulp for Botryosphaereacea species). The distribution of CRRD symptoms indicated the presence of quantitative inheritance. The direct selection of the 15 more resistant accessions based on the genotypic predicted values result in high reductions of disease (>50%). However, there was a low matching rate of the most resistant accessions for each pathogen and the different parts of the tuberous roots (peel and pulp). The CI and MI were the most promising compared to the SRI to ensure high and balanced resistance for each pathogen. Understanding the genetic basis of resistance to CRRD and the identification of sources with multiple resistance may be useful in various management strategies to control the disease.     

不同品种及有关外因对水稻纹枯病抗性的影响

选择9个具不同纹枯病抗性的水稻品种，采用3个纹枯病菌株和2种接种方法，在2个生长季进行水稻品种纹枯病抗性的综合评价。结果表明，生长季、接种方法和菌株极显著地影响水稻品种对纹枯病的抗性反应，其中，以生长季因子的效应最大。不同接种方法对水稻纹枯病发病程度的影响因生长季的不同有所变化。不同品种在同一生长季、接     

A SNP mutation affects rhizomania-virus content of sugar beets grown on resistance-breaking soils

Rhizomania is one of the most devastating biotic stresses affecting sugar beet (Beta vulgaris L.). It is caused by Beet necrotic yellow vein virus (BNYVV) vectored by the plasmodiophorid Polymyxa betae K. The only means available to control the disease is the use of genetically resistant varieties. “Rizor” or “Holly” (Rz1) and WB42 (Rz2) have been the most widely used resistance sources in the commercial varieties. Recently, naturally occurring resistance-breaking (RB) rhizomania strains have been identified causing major concerns. The aim of this study was to identify SNP mutations that show associations with resistance to rhizomania in sugar beet plants grown under resistance-breaking (RB)-BNYVV soils. Rhizomania virus content was evaluated by indirect triple-antibody sandwich-ELISA within two F ₂ segregating populations respectively grown on an AYPR and IV-BNYVV strain infected soils. Bulked segregant analysis (BSA) was performed. The resistant and susceptible plants were genotyped with a 384-SNPs panel. Of the 384 SNPs, SNP249 was found to associate with the resistance both to the AYPR strain (R ² = 0.37; P = 0.0004) and to the IV-BNYVV (R ² = 0.09; P = 0.0074). Our results suggested that the SNP249 could be readily applicable for marker-assisted breeding of resistance to AYPR strain of rhizomania.     

Inhibition of rice (Oryza sativa L.) seedling elongation by a Pseudomonas fuscovaginae toxin

Summary The effects of a Pseudomonas fuscovaginae toxin, on germination, root formation and seedling elongation, after soaking rice grains in the toxin prior to sowing, was investigated. The toxin enhanced germination, but had no apparent effect on the number of roots of the seedlings. It induced a drastic inhibition of seedlings elongation correlated to varieties susceptibility to the disease in the rice field. After denaturation of the bioactive compounds of the extract, all the previously observed effects were lost. Using the toxin and the present test, could be a reliable tool for screening genotype susceptibility to P. fuscovaginae disease.     

抗水稻纹枯病qSB-9Tq基因效应及作用方式分析

水稻第9染色体上存在1个抗纹枯病QTL,被命名为qSB-9,水稻品种特青在该QTL上携带抗性等位基因qSB-9^Tq,而Lemont携带相对感病等位基因qSB-9^Le。为精确地评价qSB-9^Tq的抗病效应,分析其作用方式,利用分子标记进行前景选择和背景选择,从轮回亲本Lemont与特青回交后代群体中筛选到1个目标单株。连续3年对该单株的扩繁后代(BC₆F₂)及随后获得的近等基因系采用嵌入法进行接种鉴定试验。田间试验采取2种不同的设计。第一种是完全随机试验,即从BC₆F₂分离群体中筛选出目标区间为qSB-9^TqTq纯合型、qSB-9^LeLe纯合型和qSB-9^TqLe杂合型个体,并对3种基因型个体间的病级平均数差异进行统计分析。第二种设计为随机区组设计,即在BC₆F₃和BC₆F₄代,分别对上述3种基因型的近等基因系群体,按3次重复的随机区组设计进行移栽和接种鉴定试验。结果表明,3年的试验结果表现出一致的趋势,即qSB-9^Tq存在于分子标记RM242~Y92.5之间,可减轻病级1.0级(0~9级病情分级系统)左右,且其抗性表现为几乎完全的显性特征。本研究的结果为qSB-9^Tq的精细定位和育种利用奠定了基础。     

Combining ability and GGE biplot analyses for resistance to northern leaf blight in tropical and subtropical elite maize inbred lines

The incidence and severity of northern leaf blight (NLB) disease has increased in Southern Africa in the past years with previously resistant cultivars being affected; implying more resistant sources have to be identified and inheritance of NLB resistance investigated. Therefore, 45 F₁ hybrids generated in a half diallel mating of ten elite maize inbred lines were evaluated in six environments for combining ability, genotype × environment interaction and effect of NLB disease on grain yield. General and specific combining ability (GCA and SCA) were highly significant (P < 0.001) for both NLB disease and grain yield. The GCA/SCA ratio was close to unity for both NLB (0.96) and grain yield (0.89), indicating predominance of additive over non-additive gene action for the traits in these inbred lines. Parent P2 and P7 had good GCA for both NLB disease resistance and high grain yield. The NLB disease ratings on the maize hybrids and inbreds ranged from 1.0 to 8.5 (approximately 0–75 % severity). Negative slope coefficients of the linear regression indicated maize yield decrease of 280–610 kg ha^?1 for NLB final disease severity of about 25–75 %, respectively, stressing the need for resistant cultivars to manage the disease. Genotype and (genotype × environment) (GGE) biplots indicated absence of crossover interaction and revealed positive associations among environments, signifying the suitability of all the environments for disease screening. Therefore, the significant additive effects for NLB disease and grain yield entail that breeding progress would be made through selection and a few disease ‘hot-spot’ sites, such as Cedara (South Africa) and Mpongwe (Zambia) can be used for disease screening.