甜玉米小斑病抗性的遗传分析与主效QTL定位

为培育抗病品种,利用抗小斑病甜玉米自交系T14和感小斑病自交系T18为亲本配制杂交组合,对玉米抗小斑病性状进行遗传分析和抗病基因分子标记定位,用主基因＋多基因混合遗传模型和P₁、P₂、F₁、B₁、B₂、F₂ 6世代联合分析的方法对单位叶面积病斑数量进行遗传分析,并应用复合区间作图法检测抗小斑病QTL。结果表明,单位叶面积病斑数量受2对加性-显性-上位性主基因控制,自交系T14的抗病性在各个分离世代都以主基因遗传为主。在第4染色体上检测到4个相互连锁的小斑病抗性QTL,解释表型变异的7.7%、30.9%、14.8%和11.5%;在第6染色体上定位了1个抗病QTL,可解释表型变异的37.7%。检测到的小斑病抗性主效QTL位于第4和第6染色体的特征与2对主基因的遗传模型相吻合。     

甘蓝型油菜蕾薹期抗旱相关性状的QTL分析

蕾薹期是甘蓝型油菜对干旱最为敏感的时期之一。以抗旱品系QY8-1和干旱敏感品种沪油16构建的含183个家系的F2∶3群体为研究材料,在现蕾至抽薹期进行干旱胁迫处理,正常灌溉为对照。结果表明,与对照相比,干旱胁迫后群体的抽薹高度、单株鲜重和叶片萎蔫指数平均下降了52.6%~55.3%,而且三个指标高度正相关。利用335个SRAP标记构建了一个长度为1661.9 c M的遗传图谱,通过复合区间作图法共检测到28个QTL,分布在14个连锁群上,可解释1.1%~36.6%的表型变异。其中,利用抽薹高度共检测到10个QTL,位于第15连锁群的q SH-D-5可解释36.6%的表型变异,为主效QTL。该区间还检测到其它3个QTL(q SH-DRI-1、q SH-D-5和q LWI-D-1),在抗旱分子标记辅助选择中应予以重点关注。同样,在第16连锁群(标记区间Em01/Me12-1—Em01Me09-1)也检测到4个重合的QTL,贡献率为1.1%~8.1%,为微效QTL。     

北方旱寒区冬油菜抗寒性相关指标的QTL定位

以抗寒性不同的白菜型冬油菜品种陇油7号与陇油9号为亲本构建的F2群体为材料,对白菜型冬油菜抗寒性相关的生理指标进行了QTL定位分析。在白菜型油菜的10条染色体上定位了SOD活性、POD活性、CAT活性、MDA含量、游离脯氨酸含量和可溶性蛋白含量共6个性状的24个QTL位点,可解释表型变异为11.1783%~81.1753%;10个显性效应表现为显性正效应,LOD值在3.2787~163.7958之间。染色体2A的Br ID90127-Br ID10421区、Br ID10421-Br ID10709区及Br ID10709-Br ID101165区,5A的BRMS034(R5)-Ra3-H10区、6A的Ra1-F06-Ra2-D04区、8A的Br ID10839-Ra2-E12区和10A的Br ID90115-Ra2-E07区是多个性状QTL共享的标记区间。研究结果对冬油菜抗寒性基因精确定位具有一定价值。     

187份玉米自交系抗旱性评价及SSR标记关联分析

在正常供水(CK)及干旱胁迫处理(S)下测定187份玉米自交系的株高、穗位高、穗位比、雄穗分枝数、散粉-吐丝时间间隔(ASI)及雌穗个数6个农艺性状,综合评价相应自交系的抗旱性强弱;采用145对SSR标记通过关联分析检测不同水旱环境下与玉米这6个农艺性状显著关联的分子标记。结果表明:干旱胁迫下187份玉米自交系农艺性状除ASI显著增大外,其余5个农艺性状均显著降低,且干旱胁迫下这些性状的变化幅度介于-72.73%～11.96%;以株高、穗位高、穗位比、雄穗分枝数、散粉-吐丝时间间隔(ASI)及雌穗个数6个性状的抗旱系数作为玉米抗旱性评价指标,并采用隶属函数法筛选出强抗旱自交系45份、中等抗旱自交系74份、旱敏感自交系68份。用一般线性模型(GLM)在不同水旱环境下共检测到了13个SSR位点与这6个性状在P0.01水平显著关联,其主要位于第1、2、3、4、5、7、8及9号染色体上,单个位点可解释表型变异的2.15%～17.13%,大约85.19%的SSR位点可在干旱胁迫环境下检测到;其中bnlg149 (Bin 1.01)、phi053 (Bin 3.05)、umc1621a (Bin 4.06)、umc1155 (Bin 5.05)、umc1072 (Bin 5.07)及umc1120 (Bin 9.04)等6个SSR与不同水旱环境下的多个农艺性状同时连锁,表现出明显的一因多效现象。     

水稻稻瘟病抗性QTL的定位分析

 稻瘟病是危害水稻最严重的病害之一。以抗稻瘟病的云南省地方品种魔王谷（MWG）和感稻瘟病的湖北省审定品种鄂晚8号（EW8）为亲本材料,构建双单倍体分离群体（DH）。利用22个菌株对亲本材料MWG/EW8进行致病性鉴定,从中筛选到5个毒性不同的鉴别菌株用于考察DH群体的稻瘟病抗性,构建包含120对SSR标记的分子遗传连锁图进行数量性状位点（QTL）的分析,鉴定出3个抗性QTL,均位于第6染色体长臂RM541附近, 3个QTL对抗病表型的贡献率介于7.7%~15.2 %之间,3个QTL的抗病等位基因均源自亲本MWG。     

四倍体马铃薯SSR遗传图谱的构建及晚疫病抗性QTL初步定位

利用四倍体马铃薯栽培种‘大西洋'和‘陇薯6号'杂交得到的190个F_1株系为作图群体,构建了四倍体马铃薯的分子遗传图谱,采用区间作图法对马铃薯晚疫病抗性进行了QTL初步定位。结果显示:通过对190个F_1株系进行检测,共发现有7个与晚疫病抗性相关的QTL位点,分别分布在第5、6、7、10和11连锁群上;各位点的LOD值在2.70~10.32之间,其中主效QTL位点3个(LOD≥3.5),可解释17.37%~65.68%的表型变异。获得紧密连锁的特异标记(S183-210、S148-460)为进一步进行QTL精确定位提供了参考。     

湘资3150 微效抗瘟性基因鉴定

 以湘资3150 和CO39 为亲本建立F10 重组自交系群体为材料, 在桃江病圃应用自然诱发接种法对群体的田间叶瘟抗性表现进行了分析。结果表明, 在LOD 2. 5 的域值上,共检测到14 个有效的微效基因QTL 位点(LOD 值均大于2. 5),分别位于水稻第3、8 和10 染色体上,其表型变异贡献值差异比较大,介于11. 78% ~ 40. 57% 之间;表明可能控制不同抗性表型的QTL 紧密连锁或者同一个QTL 对不同的抗性表型均具有抗性贡献。     

水稻异株克生抗杂草的数量性状及其基因定位研究

水稻异株克生抗杂草的特性是受数量性状控制的。异株克生抗靶杂草水稻材料与非异株克生抗靶杂草的杂种二代 (F₂)经生物检测 ,靶杂草的根或芽长的表型呈现正态分布。通过常规育种很难获得更强的异株克生作用亲本的杂种 ,因与水稻异株克生相关的效应基因数不多。目前唯一的有关水稻异株克生基因定位的研究报道表明 ,有 4个数量性状位点 (QTLs)分别位于第 2、3、3、8条染色体上。异株克生主效应的QTLs与根形态的主效应不在同一个位点。对产生异株克生物质的酶作定位标记 ,可对QTLs作进一步精细定位 ,最终实现异株克生作用的基因克隆     

陆地棉对黄萎病抗性的分子标记研究

 利用陆地棉标准系TM-1和常抗棉2个陆地棉品种杂交并自交,获得109个F₂单株及F_2:3家系为作图群体,以SSR、RAPD和SRAP 3种分子标记进行抗黄萎病性状的分子标记筛选。结果从1611对(条)引物中仅筛选到70对(条)多态性引物,获得75个多态性位点并进行标记间的连锁性分析。75个标记构建了一个包括15个连锁群,全长535 cM的陆地棉品种间分子标记遗传连锁图,标记间平均距离为11.15 cM,有27个标记不能进入任何连锁群。连锁群的标记数最少2个,最多6个;长度从1.0 cM到92.7 cM不等。对其F_2:3家系的成株期抗黄萎病性状即平均病情指数的分布进行分析,显示其呈正态分布,进一步说明陆地棉对黄萎病的抗性为数量遗传;单标记分析及复合区间作图,检测出与抗黄萎病性相关的3个QTL,分别位于第3、5、6连锁群上,贡献率分别为14.15%、3.45%和18.78%。另外,对该群体生长过程中黄萎病不同发病高峰期的病情也进行了分析。     

深松耕作对不同年代玉米品种生理成熟后的抗倒伏力学特性的影响

以1970—2010s主推玉米品种为材料,设置深松与浅旋耕处理,研究深松耕作对不同年代玉米品种生理成熟后的抗倒伏力学特征的影响。结果表明,生理成熟后玉米倒伏率增加;与浅旋耕相比,深松耕作使不同玉米品种的茎折率平均降低1.22个百分点,茎秆力学强度增加;高密度下玉米茎秆力学强度的增幅更加明显,1970s品种第4节间压碎强度增加了43.6%、第5节间弯曲强度增加了33.05%;1980s品种第3～5节间穿刺强度和第3、5节间弯曲强度、1990s品种第4节间压碎强度和第3节间弯曲强度、2000s品种第3～5节间穿刺强度和第3节间弯曲强度也有明显增加;而2010s品种在深松高密与浅旋高密下,茎秆力学强度指标无明显变化。深松耕作对玉米群体生理成熟后抗倒性的提高与第3、4节间穿刺强度、第4节间弯曲强度和第3、5节间压碎强度的增加密切相关;但随着品种演替茎秆力学强度无明显增强,第3节间穿刺强度以0.26×10⁷ N·m^-2·10a^-1的速率降低。由此可见,茎秆力学强度可作为构建玉米抗倒伏群体的指标,但评价品种抗茎折能力具有一定片面性,...     

Identification of isolate‐specific resistance QTLs to phytophthora root rot using an intraspecific recombinant inbred line population of pepper (Capsicum annuum)

Quantitative trait loci (QTL) for resistance to phytophthora root rot caused by Phytophthora capsici were investigated using two Korean P. capsici isolates and 126 F₈ recombinant inbred lines derived from a cross of Capsicum annuum line YCM334 (resistant parent) and local cv. Tean (susceptible parent). The experimental design was a split plot with two replications. Highly significant effects of pathogen isolate, plant genotype, and genotype × isolate were detected. QTL mapping was performed using a genetic linkage map covering 1486·6 cM of the pepper genome, and consisted of 249 markers including 136 AFLPs (Amplified Fragment Length Polymorphisms), 112 SSRs (Simple Sequence Repeats) and one CAPS (Cleaved Amplified Polymorphic Sequence). Fifteen QTLs were detected on chromosomes 5 (P5), 10 (P10), 11 (P11), Pb and Pc using two data processing methods: percentage of wilted plants (PWP) and relative area under the disease progress curves (RAUDPC). The phenotypic variation explained by each QTL (R²) ranged from 6·0% to 48·2%. Seven QTLs were common to resistance for the two isolates on chromosome 5 (P5); six were isolate‐specific for isolate 09‐051 on chromosomes 10 (P10) and Pc, and two for isolate 07‐127 on chromosomes 11 (P11) and Pb. The QTLs in common with the major effect on the resistance for two isolates explained 20·0–48·2% of phenotypic variation. The isolate‐specific QTLs explained 6·0–17·4% of phenotypic variation. The result confirms a gene‐for‐gene relationship between C. annuum and P. capsici for root rot resistance.     

QTLs for potato tuber resistance to Dickeya solani are located on chromosomes II and IV

The goal of this research was to identify quantitative trait loci (QTLs) for potato tuber resistance to the soil- and seedborne bacterium Dickeya solani and for tuber starch content, to study the relationship between these traits. A resistant diploid hybrid of potato, DG 00-270, was crossed with a susceptible hybrid, DG 08-305, to generate the F₁ mapping population. Tubers that were wound-inoculated with bacteria were evaluated for disease severity, expressed as the mean weight of rotted tubers, and disease incidence, measured as the proportion of rotten tubers. Diversity array technology (DArTseq) was used for genetic map construction and QTL analysis. The most prominent QTLs for disease severity and incidence were identified in overlapping regions on potato chromosome IV and explained 22.4% and 22.9% of the phenotypic variance, respectively. The second QTL for disease severity was mapped to chromosome II and explained 16.5% of the variance. QTLs for starch content were detected on chromosomes III, V, VI, VII, VIII, IX, XI, and XII in regions different from the QTLs for soft rot resistance. Two strong and reproducible QTLs for resistance to D. solani on potato chromosomes IV and II might be useful for further study of candidate genes and marker development in potato breeding programmes. The relationship between tuber resistance to bacteria and the starch content in potato tubers was not confirmed by QTL mapping, which makes the selection of genotypes highly resistant to soft rot with a desirable starch content feasible.     

Main effects, epistasis, and environmental interactions of quantitative trait Loci for fusarium head blight resistance in a recombinant inbred population

ABSTRACT Chinese Spring Sumai 3 chromosome 7A disomic substitution line (CS-SM3-7ADS) is highly resistant to Fusarium head blight (FHB), and an F(7) population of recombinant inbred lines derived from the cross CS-SM3-7ADS x Annong 8455 was evaluated for resistance to FHB to investigate main effects, epistasis, and environmental interactions of quantitative trait loci (QTLs) for FHB resistance. A molecular linkage map consists of 501 simple sequence repeat and amplified fragment length polymorphism markers. A total of 10 QTLs were identified with significant main effects on the FHB resistance using MapQTL and QTLMapper software. Among them, CS-SM3-7ADS carries FHB-resistance alleles at five QTLs on chromosomes 2D, 3B, 4D, and 6A. One QTL on 3BS had the largest effect and explained 30.2% of the phenotypic variance. Susceptible QTLs were detected on chromosomes 1A, 1D, 4A, and 4B. A QTL for enhanced FHB resistance was not detected on chromosome 7A of CS-SM3-7ADS; therefore, the increased FHB resistance in CS-SM3-7ADS was not due to any major FHB-resistance QTL on 7A of Sumai 3, but more likely was due to removal of susceptible alleles of QTLs on 7A of Chinese Spring. QTLMapper detected nine pairs of additive-additive interactions at 17 loci that explained 26% phenotypic variance. QTL-environment interactions explained 49% of phenotypic variation, indicating that the environments significantly affected the expression of the QTLs, especially these epistasis QTLs. Adding FHB-enhancing QTLs or removal of susceptible QTLs both may significantly enhance the degree of wheat resistance to FHB in a wheat cultivar.     

Quantitative trait loci conferring blast resistance in hexaploid wheat at adult plant stage

Blast disease, caused by the Magnaporthe oryzae Triticum pathotype (MoT), is a major concern for wheat production in tropical and subtropical regions. The most destructive symptoms occur in wheat spikes. Infected spikes become bleached due to partial or total sterility, producing small and wrinkled grains. High disease pressure of the disease results in significant yield losses. This study aimed to identify wheat quantitative trait loci (QTLs) conferring resistance to blast disease at the heading stage. A doubled-haploid population was developed from the cross between BRS 209 (susceptible) and CBFusarium ENT014 (resistant, carrying the 2NS translocation). A linkage map was constructed containing 5,381 molecular markers and the inclusive composite interval mapping method was employed for QTL detection. Four QTLs were mapped in response to two MoT isolates. The major QTL identified on the 2AS chromosome explained an average of 84.0% of the phenotypic variation for spike bleaching at 9 days postinoculation and reinforces the potency of the 2NS translocation. Recombination between the distal region of chromosome 2AS and the 2NS marker was found. These results could explain why some lines carrying the VENTRIUP/LN2 marker have a variable reaction to the disease. QTLs on 5B and 7B chromosomes were also identified. Two mechanisms of resistance were hypothesized: the hypersensitive response and resistance to colonization of host tissues. The KASP markers thus developed and simple sequence repeats (SSRs) allocated in QTL regions can be used in the future for the development of wheat blast-resistant cultivars.     

Mapping quantitative trait Loci for resistance to rice blast

Quantitative trait loci (QTLs) conferring resistance to rice blast, caused by Magnaporthe oryzae, have been under-explored. In the present study, composite interval mapping was used to identify the QTLs that condition resistance to the 6 out of the 12 common races (IB1, IB45, IB49, IB54, IC17, and ID1) of M. oryzae using a recombinant inbred line (RIL) population derived from a cross of the moderately susceptible japonica cultivar Lemont with the moderately resistant indica cultivar Jasmine 85. Disease reactions of 227 F(7) RILs were determined using a category scale of ratings from 0, representing the most resistant, to 5, representing the most susceptible. A total of nine QTLs responsive to different degrees of phenotypic variation ranging from 5.17 to 26.53% were mapped on chromosomes 3, 8, 9, 11, and 12: qBLAST3 at 1.9 centimorgans (cM) to simple sequence repeat (SSR) marker RM282 on chromosome 3 to IB45 accounting for 5.17%; qBLAST8.1 co-segregated with SSR marker RM1148 to IB49 accounting for 6.69%, qBLAST8.2 at 0.1 cM to SSR marker RM72 to IC17 on chromosome 8 accounting for 7.22%; qBLAST9.1 at 0.1 cM to SSR marker RM257 to IB54, qBLAST9.2 at 2.1 cM to SSR marker RM108, and qBLAST9.3 at 0.1 cM to SSR marker RM215 to IC17 on chromosome 9 accounting for 4.64, 7.62, and 4.49%; qBLAST11 at 2.2 cM to SSR marker RM244 to IB45 and IB54 on chromosome 11 accounting for 26.53 and 19.60%; qBLAST12.1 at 0.3 cM to SSR marker OSM89 to IB1 on chromosome 12 accounting for 5.44%; and qBLAST12.2 at 0.3 and 0.1 cM to SSR marker OSM89 to IB49 and ID1 on chromosome 12 accounting for 9.7 and 10.18% of phenotypic variation, respectively. This study demonstrates the usefulness of tagging blast QTLs using physiological races by composite interval mapping.     

DArTseq physical mapping of QTLs linked to Karnal bunt (Tilletia indica) resistance in two historical wheat populations

Karnal bunt, a disease of wheat, durum, rye, and triticale, is subject to strict quarantine restrictions worldwide. The disease is considered a major threat to food security, due to its use as a non-tariff trade barrier by several wheat-importing countries. In this paper, we analysed seven years of phenotypic data to search for quantitative trait loci (QTLs) associated with resistance in common wheat, validated the QTLs using an independent population, and assessed the potential of genomic selection as a tool for pre-emptive breeding. The QTL study used phenotypic data collected from artificially inoculated field experiments involving two historical Karnal bunt resistance populations: WH542 × HD29 and WH542 × W485. QTL analyses detected four significant (p < 0.001) QTLs on chromosomes 1A, 3A, 4B, and 6B, which explained between 13.7% and 15.7% of the phenotypic variation. A panel of 130 cultivars was used to validate QTL effects. These were genotyped with the same DArTseq protocol, and two of the four QTLs were significantly (p < 0.001) associated with Karnal bunt resistance in the validation panel. The potential of genomic selection was investigated by comparing accuracies of a model trained with all available markers and a model based solely on validated QTL information from the biparental populations. Genomic prediction accuracy, based on the two scenarios, averaged 0.43 and 0.33, respectively, suggesting that even in situations where phenotyping is difficult due to quarantine restrictions, the prospects for pre-emptive breeding against Karnal bunt are encouraging, and resources are now available that will reduce the cost burden.     

Identification and Mapping of Quantitative Trait Loci Conditioning Resistance to Southern Leaf Blight of Maize Caused by Cochliobolus heterostrophus Race O

ABSTRACT A random set of recombinant inbred (RI) lines (F2:7) derived from the cross of the inbred lines Mo17 (resistant) and B73 (susceptible) were evaluated for resistance to southern leaf blight (SLB) caused by Cochliobolus heterostrophus race O. The RI lines were genotyped at a total of 234 simple sequence repeat, restriction fragment length polymorphism, or isozyme loci. Field plots of the RI lines were inoculated artificially with an aggressive isolate of C. heterostrophus race O in each of two growing seasons in North Carolina. Lines were rated for percent SLB severity two (1996) or three (1995) times during the grain-filling period. Data also were converted to area under the disease progress curve (AUDPC) and analyzed using the composite interval mapping option of the PLABQTL program. When means of disease ratings over years were fitted to models, a total of 11 quantitative trait loci (QTLs) were found to condition resistance to SLB, depending upon which disease ratings were used in the analyses. When the AUDPC data were combined and analyzed over environments, seven QTLs, on chromosomes 1, 2, 3, 4, 7, and 10 were found to come from the resistant parent Mo17. An additional QTL for resistance on chromosome 1 came from the susceptible parent B73. The eight identified QTLs accounted for 46% of the phenotypic variation for resistance. QTL x environment interactions often were highly significant but, with one exception, were the result of differences in the magnitude of QTL effects between years and not due to changes in direction of effects. QTLs on the long arm of chromosome 1 and chromosomes 2 and 3 had the largest effects, were the most consistently detected, and accounted for most of the phenotypic variance. No significant additive x additive epistatic effects were detected. These data support earlier reports of the polygenic inheritance of resistance to SLB of maize.     

Molecular mapping of the blast resistance genes Pi2-1 and Pi51(t) in the durably resistant rice 'Tianjingyeshengdao'

Tianjingyeshengdao' (TY) is a rice cultivar with durable resistance to populations of Magnaporthe oryzae (the causal agent of blast) in China. To understand the genetic basis of its resistance to blast, we developed a population of recombinant inbred lines from a cross between TY and the highly susceptible 'CO39' for gene mapping analysis. In total, 22 quantitative trait loci (QTLs) controlling rice blast resistance were identified on chromosomes 1, 3, 4, 5, 6, 9, 11, and 12 from the evaluation of four disease parameters in both greenhouse and blast nursery conditions. Among these QTLs, 19 were contributed by TY and three by CO39. Two QTL clusters on chromosome 6 and 12 were named Pi2-1 and Pi51(t), respectively. Pi2-1 was detected under both growth chamber and natural blast nursery conditions, and explained 31.24 to 59.73% of the phenotypic variation. Pi51(t) was only detected in the natural blast nursery and explained 3.67 to 10.37% of the phenotypic variation. Our results demonstrate that the durable resistance in TY is controlled by two major and seven minor genes. Identification of the markers linked to both Pi2-1 and Pi51(t) in this study should be useful for marker-aided selection in rice breeding programs as well as for molecular cloning of the identified resistance genes.