Identification of a major quantitative trait locus for resistance to maize rough dwarf virus in a Chinese maize inbred line X178 using a linkage map based on 514 gene-derived single nucleotide polymorphisms

Maize rough dwarf disease (MRDD) is a worldwide viral disease and causes significant yield losses in maize (Zea mays L.) production. In this study, we mapped and characterized quantitative trait loci (QTL) conferring resistance to MRDD using 89 F8 recombinant inbred lines derived from a cross between X178 (resistant parent) and B73 (susceptible). The population was evaluated for MRDD resistance in Baoding, Hebei Province, China (a hot spot of MRDD incidence) under natural infection in 2008 and 2009 and artificial inoculation in 2010. Genotypic variances for disease severity index (DSI) were highly significant in the population. Heritability estimates for DSI evaluation were 0.472 and 0.467 in 2008 and 2009, respectively. The linkage map was constructed using 514 gene-derived single nucleotide polymorphisms (SNPs) and 72 simple sequence repeat markers, spanning a genetic distance of 1,059.72?cM with an average interval of 1.8?cM between adjacent markers. Multiple-QTL model mapping detected a major QTL for MRDD resistance on chromosome 8, explaining 24.6?C37.3% of the phenotypic variation across three environments. In 2010, an additional QTL was detected on chromosome 10, explaining 15.8% of the phenotypic variation. The major QTL on chromosome 8 and the SNP markers (SNP31, SNP548, and SNP284) co-located with the QTL peak have potential for further functional genomic analysis and use in molecular marker-assisted selection for MRDD resistance in maize.     

Enhanced Virus Resistance in Transgenic Maize Expressing a dsRNA-Specific Endoribonuclease Gene from E. coli

Maize rough dwarf disease (MRDD), caused by several Fijiviruses in the family Reoviridae, is a global disease that is responsible for substantial yield losses in maize. Although some maize germplasm have low levels of polygenic resistance to MRDD, highly resistant cultivated varieties are not available for agronomic field production in China. In this work, we have generated transgenic maize lines that constitutively express rnc70, a mutant E. coli dsRNA-specific endoribonuclease gene. Transgenic lines were propagated and screened under field conditions for 12 generations. During three years of evaluations, two transgenic lines and their progeny were challenged with Rice black-streaked dwarf virus (RBSDV), the causal agent of MRDD in China, and these plants exhibited reduced levels of disease severity. In two normal years of MRDD abundance, both lines were more resistant than non-transgenic plants. Even in the most serious MRDD year, six out of seven progeny from one line were resistant, whereas non-transgenic plants were highly susceptible. Molecular approaches in the T12 generation revealed that the rnc70 transgene was integrated and expressed stably in transgenic lines. Under artificial conditions permitting heavy virus inoculation, the T12 progeny of two highly resistant lines had a reduced incidence of MRDD and accumulation of RBSDV in infected plants. In addition, we confirmed that the RNC70 protein could bind directly to RBSDV dsRNA in vitro. Overall, our data show that RNC70-mediated resistance in transgenic maize can provide efficient protection against dsRNA virus infection.     

玉米粗缩病的分子研究新进展

粗缩病是一种世界性玉米(Zea mays)病害,造成玉米产量降低和品质下降。已有的研究表明,导致玉米粗缩病的病毒有4种,均属于植物呼肠孤病毒科、斐济病毒属(Fijivirus)第2组的成员,它们的全基因组均由10条双链RNA片段组成,编码13个蛋白分子;迄今未发现对粗缩病完全免疫的研究材料,但已筛选出少量在不同环境下均表现高抗的种质。玉米抗粗缩病为多基因控制的数量性状,每条染色体上均有可能存在与粗缩病抗性有关的基因座(QTLs)。粗缩病毒侵染玉米后,引起细胞防御系统中相关基因表达、蛋白质合成和激素含量等生物途径发生变化。该文对玉米粗缩病病原分子特征和遗传变异、抗性种质遗传基础及致(抗)病机理等方面的研究成果进行了阐述,旨在为玉米抗粗缩病分子育种提供理论依据。     

Selection mapping of loci for quantitative disease resistance in a diverse maize population

The selection response of a complex maize population improved primarily for quantitative disease resistance to northern leaf blight (NLB) and secondarily for common rust resistance and agronomic phenotypes was investigated at the molecular genetic level. A tiered marker analysis with 151 simple sequence repeat (SSR) markers in 90 individuals of the population indicated that on average six alleles per locus were available for selection. An improved test statistic for selection mapping was developed, in which quantitative trait loci (QTL) are identified through the analysis of allele-frequency shifts at mapped multiallelic loci over generations of selection. After correcting for the multiple tests performed, 25 SSR loci showed evidence of selection. Many of the putatively selected loci were unlinked and dispersed across the genome, which was consistent with the diffuse distribution of previously published QTL for NLB resistance. Compelling evidence for selection was found on maize chromosome 8, where several putatively selected loci colocalized with published NLB QTL and a race-specific resistance gene. Analysis of F(2) populations derived from the selection mapping population suggested that multiple linked loci in this chromosomal segment were, in part, responsible for the selection response for quantitative resistance to NLB.     

Discovery and validation of genomic regions associated with resistance to maize lethal necrosis in four biparental populations

In sub-Saharan Africa, maize is the key determinant of food security for smallholder farmers. The sudden outbreak of maize lethal necrosis (MLN) disease is seriously threatening the maize production in the region. Understanding the genetic basis of MLN resistance is crucial. In this study, we used four biparental populations applied linkage mapping and joint linkage mapping approaches to identify and validate the MLN resistance-associated genomic regions. All populations were genotyped with low to high density markers and phenotyped in multiple environments against MLN under artificial inoculation. Phenotypic variation for MLN resistance was significant and heritability was moderate to high in all four populations for both early and late stages of disease infection. Linkage mapping revealed three major quantitative trait loci (QTL) on chromosomes 3, 6, and 9 that were consistently detected in at least two of the four populations. Phenotypic variance explained by a single QTL in each population ranged from 3.9% in population 1 to 43.8% in population 2. Joint linkage association mapping across three populations with three biometric models together revealed 16 and 10 main effect QTL for MLN-early and MLN-late, respectively. The QTL identified on chromosomes 3, 5, 6, and 9 were consistent with the QTL identified by linkage mapping. Ridge regression best linear unbiased prediction with five-fold cross-validation revealed high accuracy for prediction across populations for both MLN-early and MLN-late. Overall, the study discovered and validated the presence of major effect QTL on chromosomes 3, 6, and 9 which can be potential candidates for marker-assisted breeding to improve the MLN resistance.     

Mapping of QTL associated with waterlogging tolerance during the seedling stage in maize

BACKGROUND AND AIMS: Soil waterlogging is a major environmental stress that suppresses maize (Zea mays) growth and yield. To identify quantitative trait loci (QTL) associated with waterlogging tolerance at the maize seedling stage, a F2 population consisting of 288 F(2:3) lines was created from a cross between two maize genotypes, 'HZ32' (waterlogging-tolerant) and 'K12' (waterlogging-sensitive). METHODS: The F2 population was genotyped and a base-map of 1710.5 cM length was constructed with an average marker space of 11.5 cM based on 177 SSR (simple sequence repeat) markers. QTL associated with root length, root dry weight, plant height, shoot dry weight, total dry weight and waterlogging tolerance coefficient were identified via composite interval mapping (CIM) under waterlogging and control conditions in 2004 (EXP.1) and 2005 (EXP.2), respectively. KEY RESULTS AND CONCLUSIONS: Twenty-five and thirty-four QTL were detected in EXP.1 and EXP.2, respectively. The effects of each QTL were moderate, ranging from 3.9 to 37.3 %. Several major QTL determining shoot dry weight, root dry weight, total dry weight, plant height and their waterlogging tolerance coefficient each mapped on chromosomes 4 and 9. These QTL were detected consistently in both experiments. Secondary QTL influencing tolerance were also identified and located on chromosomes 1, 2, 3, 6, 7 and 10. These QTL were specific to particular traits or environments. Although the detected regions need to be mapped more precisely, the findings and QTL found in this study may provide useful information for marker-assisted selection (MAS) and further genetic studies on maize waterlogging tolerance.     

QTL mapping of resistance to Fusarium ear rot using a RIL population in maize

Fusarium ear rot is a prevalent disease in maize, reducing grain yields and quality. Resistance breeding is an efficient way to minimize losses caused by the disease. In this study, 187 lines from a RIL population along with the resistant (87-1) and susceptible (Zong 3) parents were planted in Zhengzhou and Beijing with three replications in years 2004 and 2006. Each line was artificially inoculated using the nail-punch method. Significant genotypic variation in response to Fusarium ear rot was detected in both years. Based on a genetic map containing 246 polymorphic SSR markers with average genetic distances of 9.1 cM, the ear-rot resistance QTL were firstly analyzed by composite interval mapping (CIM). Three QTL were detected in both Zhengzhou and Beijing in 2004; and three and four QTL, respectively, were identified in 2006. The resistant parent contributed all resistance QTL. By using composite interval mapping and a mixed model (MCIM), significant epistatic effects on Fusarium ear rot as well as interactions between mapped loci and environments were observed across environments. Two QTL on chromosome 3 (3.04 bin) were consistently identified across all environments by the two methods. The major resistant QTL with the largest effect was flanked by markers umc1025 and umc1742 on chromosome 3 (3.04 bin), explaining 13–22% of the phenotypic variation. The SSR markers closely flanking the major resistance QTL will facilitate marker-assisted selection (MAS) of resistance to Fusarium ear rot in maize breeding programs.     

Identification of quantitative trait loci (QTL) for resistance to Fusarium crown rot (Fusarium pseudograminearum) in multiple assay environments in the Pacific Northwestern US

Fusarium crown rot (FCR), caused by Fusarium pseudograminearum and F. culmorum, reduces wheat (Triticum aestivum L.) yields in the Pacific Northwest (PNW) of the US by as much as 35%. Resistance to FCR has not yet been discovered in currently grown PNW wheat cultivars. Several significant quantitative trait loci (QTL) for FCR resistance have been documented on chromosomes 1A, 1D, 2B, 3B, and 4B in resistant Australian cultivars. Our objective was to identify QTL and tightly linked SSR markers for FCR resistance in the partially resistant Australian spring wheat cultivar Sunco using PNW isolates of F. pseudograminerarum in greenhouse and field based screening nurseries. A second objective was to compare heritabilities of FCR resistance in multiple types of disease assaying environments (seedling, terrace, and field) using multiple disease rating methods. Two recombinant inbred line (RIL) mapping populations were derived from crosses between Sunco and PNW spring wheat cultivars Macon and Otis. The Sunco/Macon population comprised 219 F(6):F(7) lines and the Sunco/Otis population comprised 151 F(5):F(6) lines. Plants were inoculated with a single PNW F. pseudograminearum isolate (006-13) in growth room (seedling), outdoor terrace (adult) and field (adult) assays conducted from 2008 through 2010. Crown and lower stem tissues of seedling and adult plants were rated for disease severity on several different scales, but mainly on a numeric scale from 0 to 10 where 0?=?no discoloration and 10?=?severe disease. Significant QTL were identified on chromosomes 2B, 3B, 4B, 4D, and 7A with LOD scores ranging from 3 to 22. The most significant and consistent QTL across screening environments was located on chromosome 3BL, inherited from the PNW cultivars Macon and Otis, with maximum LOD scores of 22 and 9 explaining 36 and 23% of the variation, respectively for the Sunco/Macon and Sunco/Otis populations. The SSR markers Xgwm247 and Xgwm299 flank these QTL and are being validated for use in marker-assisted selection for FCR resistance. This is the first report of QTL associated with FCR resistance in the US.     

Identification and mapping QTL for high-temperature adult-plant resistance to stripe rust in winter wheat (<Emphasis Type="Italic">Triticum aestivum</Emphasis> L.) cultivar ‘Stephens’

High-temperature adult-plant (HTAP) resistance from the winter wheat (Triticum aestivum) cultivar 'Stephens' has protected wheat crops from stripe rust caused by Puccinia striiformis f. sp. tritici for 30 years. The objectives of this study were to identify quantitative trait loci (QTL) for HTAP resistance in Stephens through genetic linkage analysis and identify DNA markers linked to the QTL for use in marker-assisted breeding. Mapping populations consisted of 101 recombinant inbred lines (RILs) through single-seed descent from 'Stephens' (resistant) x 'Michigan Amber' (susceptible). F(5), F(6) and F(7) RILs were evaluated for stripe rust resistance at Pullman, WA in 1996, 1997 and 1998, respectively, whereas F(8) RILs were evaluated at Mt Vernon, WA, USA in 2005. The 101 F(8) RILs were evaluated with 250 resistance gene analog polymorphism (RGAP), 245 simple sequence repeat (SSR) and 1 sequence tagged site (STS) markers for genetic linkage map construction. Two QTL, which explained 48-61% of the total phenotypic variation of the HTAP resistance in Stephens, were identified. QYrst.wgp-6BS.1 was within a 3.9-cM region flanked by Xbarc101 and Xbarc136. QYrst.wgp-6BS.2 was mapped in a 17.5-cM region flanked by Xgwm132 and Xgdm113. Both two QTL were physically mapped to the short arm of chromosome 6B, but in different bins. Validation and polymorphism tests of the flanking markers in 43 wheat genotypes indicated that the molecular markers associated with these QTL should be useful in marker-assisted breeding programs to efficiently incorporate HTAP resistance into new wheat cultivars.     

Genetic mapping of gray leaf spot (GLS) resistance genes in maize

Bulked segregant analysis was used to identify amplified fragment length polymorphism markers (AFLPs) linked to quantitative trait loci (QTLs) involved in the resistance to gray leaf spot (GLS) in maize. By using ten AFLP primer combinations 11 polymorphic markers were identified and converted to sequence- specific PCR markers. Five of the 11 converted AFLPs were linked to three GLS resistance QTLs. The markers were mapped to maize chromosomes 1, 3 and 5 using existing linkage maps of two commercially available recombinant inbred-line populations. Converted restriction fragment length polymorphism markers and microsatellite markers were used to obtain a more-precise localization for the detected QTLs. The QTL on chromosome 1 was localized in bin 1.05/06 and had a LOD score of 21. A variance of 37% was explained by the QTL. Two peaks were visible on chromosome 5, one was localized in bin 5.03/04 and the other in bin 5.05/06. Both peaks had a LOD score of 5, and 11% of the variance was explained by the QTLs. A variance of 8–10% was explained by the QTL on chromosome 3 (bin 3.04). The consistency of the QTLs was tested across two F₂ populations planted in consecutive years. Received: 10.10.00 / Accepted: 26.01.01     

Genome-Wide Association Implicates Candidate Genes Conferring Resistance to Maize Rough Dwarf Disease in Maize

Maize rough dwarf disease (MRDD) is a destructive viral disease in China, which results in 20–30% of the maize yield losses in affected areas and even as high as 100% in severely infected fields. Understanding the genetic basis of resistance will provide important insights for maize breeding program. In this study, a diverse maize population comprising of 527 inbred lines was evaluated in four environments and a genome-wide association study (GWAS) was undertaken with over 556000 SNP markers. Fifteen candidate genes associated with MRDD resistance were identified, including ten genes with annotated protein encoding functions. The homologous of nine candidate genes were predicted to relate to plant defense in different species based on published results. Significant correlation (R² = 0.79) between the MRDD severity and the number of resistance alleles was observed. Consequently, we have broadened the resistant germplasm to MRDD and identified a number of resistance alleles by GWAS. The results in present study also imply the candidate genes in defense pathway play an important role in resistance to MRDD in maize.     

烟草赤星病抗性主效QTL人工选择响应研究

分析赤星病抗性主效QTL的人工选择响应,可为烟草赤星病抗性分子标记辅助选择提供一定的理论基础。本研究利用与主效QTL紧密连锁的分子标记J9和J4,分析随机群体、人工选择群体和自然群体中响应分子标记的等位基因频率,研究相关标记位点在不同群体中的等位基因变化规律。结果发现:(1)赤星病抗性主效QTL等位基因在不同选择强度(5%、10%和20%)的正向选择条件下均发生了显著性偏分离,其中在10%的正向选择强度下偏分离显著性最高。(2)在不同世代(F3、F4、F5和F6)的赤星病抗性育种选择群体中,J9位点抗病亲本等位基因型频率显著高于感病亲本基因型频率,表明来源于抗源净叶黄的主效抗性QTL与赤星病抗性显著关联。(3)在198份自然群体中,包括烟草赤星病抗性品种中烟86、单育二号在内的50份烟草种质携带与抗源净叶黄相同的基因型,表明该主效QTL被广泛应用于烟草赤星病抗性改良中。本研究验证了之前定位到的主效抗病QTL的准确性;分析了该主效QTL的人工选择响应,相关结果为烟草赤星病抗性改良提供了一定的理论基础。     

Mapping of quantitative trait loci for kernel row number in maize across seven environments

Genetic factors controlling quantitative inheritance of grain yield and its components have been intensively investigated during recent decades using diverse populations in maize (Zea mays L.). Notwithstanding this, quantitative trait loci (QTL) for kernel row number (KRN) with large and consistent effect have not been identified. In this study, a linkage map of 150 simple sequence repeat (SSR) loci was constructed by using a population of 500 F2 individuals derived from a cross between elite inbreds Ye478 and Dan340. The linkage map spanned a total of 1478 cM with an average interval of 10.0 cM. A total of 397 F2:3 lines were evaluated across seven diverse environments for mapping QTL for KRN. Some QTL for grain yield and its components had previously been confirmed with this population across environments. A total of 13 QTL for KRN were identified, with each QTL explaining from 3.0 to 17.9% of phenotypic variance. The gene action for KRN was mainly additive to partial dominance. A large-effect QTL (qkrn7) with partial dominance effect accounting for 17.9% of the phenotypic variation for KRN was identified on chromosome 7 near marker umc1865 with consistent gene effect across seven diverse environments. This study has laid a foundation for map-based cloning of this major QTL and for developing molecular markers for marker-assisted selection of high KRN.     

QTL mapping for reaction to Phaeosphaeria leaf spot in a tropical maize population

Phaeosphaeria leaf spot (PLS) is an important disease in tropical and subtropical maize (Zea mays, L.) growing areas, but there is limited information on its inheritance. Thus, this research was conducted to study the inheritance of the PLS disease in tropical maize by using QTL mapping and to assess the feasibility of using marker-assisted selection aimed to develop genotypes resistance to this disease. Highly susceptible L14-04B and highly resistant L08-05F inbred lines were crossed to develop an F₂ population. Two-hundred and fifty six F₂ plants were genotyped with 143 microsatellite markers and their F_2:3 progenies were evaluated at seven environments. Ten plants per plot were evaluated 30 days after silk emergence following a rating scale, and the plot means were used for analyses. The heritability coefficient on a progeny mean basis was high (91.37%), and six QTL were mapped, with one QTL on chromosomes 1, 3, 4, and 6, and two QTL on chromosome 8. The gene action of the QTL ranged from additive to partial dominance, and the average level of dominance was partial dominance; also a dominance × dominance epistatic effect was detected between the QTL mapped on chromosome 8. The phenotypic variance explained by each QTL ranged from 2.91 to 11.86%, and the joint QTL effects explained 41.62% of the phenotypic variance. The alleles conditioning resistance to PLS disease of all mapped QTL were in the resistant parental inbred L08-05F. Thus, these alleles could be transferred to other elite maize inbreds by marker-assisted backcross selection to develop hybrids resistant to PLS disease.     

Precise mapping of quantitative trait loci for resistance to southern leaf blight, caused by Cochliobolus heterostrophus race O, and flowering time using advanced intercross maize lines

The intermated B73 × Mo17 (IBM) population, an advanced intercross recombinant inbred line population derived from a cross between the maize lines B73 (susceptible) and Mo17 (resistant), was evaluated in four environments for resistance to southern leaf blight (SLB) disease caused by Cochliobolus heterostrophus race O. Two environments were artificially inoculated, while two were not inoculated and consequently had substantially lower disease pressure. Four common SLB resistance quantitative trait loci (QTL) were identified in all environments, two in bin 3.04 and one each in bins 1.10 and 8.02/3. There was no significant correlation between disease resistance and days to anthesis. A direct comparison was made between SLB QTL detected in two populations, independently derived from the same parental cross: the IBM advanced intercross population and a conventional recombinant inbred line population. Several QTL for SLB resistance were detected in both populations, with the IBM providing between 5 and, in one case, 50 times greater mapping resolution.     

Genetic mapping of maize stripe disease resistance from the Mascarene source

Maize stripe virus (MStV) is a potentially threatening virus disease of maize in the tropics. We mapped quantitative trait loci (QTLs) controlling resistance to MStV in a maize population of 157 F(2:3) families derived from the cross between two maize lines, Rev81 (tropical resistant) and B73 (temperate susceptible). Resistance was evaluated under artificial inoculations in replicated screenhouse trials across different seasons in Réunion Island, France. Composite interval mapping was employed for QTL detection with a linkage map of 143 microsatellite markers. Heritability estimates across seasons were 0.96 and 0.90 for incidence and severity, respectively, demonstrating a high genotypic variability and a good control of the environment. Three regions on chromosomes 2L, 3 and 5, with major effects, and another region on chromosome 2S, with minor effects, provided resistance to MStV in Rev81. In individual seasons, the chr2L QTL explained 60-65% of the phenotypic variation for disease incidence and 21-42% for severity. The chr3 QTL, mainly associated with incidence and located near centromere, explained 42-57% of the phenotypic variation, whereas the chr5 QTL, mainly associated with severity, explained 26-53%. Overall, these QTLs explained 68-73% of the phenotypic variance for incidence and 50-59% for severity. The major QTLs on chr2 and 3 showed additive gene action and were found to be stable over time and across seasons. They also were found to be included in genomic regions with important clusters of resistance genes to diseases and pests. The major QTL on chr5 appeared to be partially dominant in favour of resistance. It was stable over time but showed highly significant QTL x season interactions. Possible implications of these QTLs in different mechanisms of resistance against the virus or the insect vector are discussed. The prospects for transferring these QTLs in susceptible maize cultivars and combining them with other resistances to virus diseases by conventional or marker-assisted breeding are promising.     

Identification of QTLs conferring resistance to downy mildews of maize in Asia

Downy mildew is one of the most destructive diseases of maize in subtropical and tropical regions in Asia. As a prerequisite for improving downy mildew resistance in maize, we analyzed quantitative trait loci (QTLs) involved in resistance to the important downy mildew pathogens--Peronosclerospora sorghi (sorghum downy mildew) and P. heteropogoni (Rajasthan downy mildew) in India, P. maydis (Java downy mildew) in Indonesia, P. zeae in Thailand and P. philippinensis in the Philippines--using a recombinant inbred line population derived from a cross between Ki3 (downy mildew resistant) and CML139 (susceptible). Resistance was evaluated as percentage disease incidence in replicated field trials at five downy mildew 'hotspots' in the four countries. Heritability estimates of individual environments ranged from 0.58 to 0.75 with an across environment heritability of 0.50. Composite interval mapping was applied for QTL detection using a previously constructed restriction fragment length polymorphism linkage map. The investigation resulted in the identification of six genomic regions on chromosomes 1, 2, 6, 7 and 10 involved in the resistance to the downy mildews under study, explaining, in total, 26-57% of the phenotypic variance for disease response. Most QTL alleles conferring resistance to the downy mildews were from Ki3. All QTLs showed significant QTL x environment interactions, suggesting that the expression of the QTL may be environment-dependent. A strong QTL on chromosome 6 was stable across environments, significantly affecting disease resistance at the five locations in four Asian countries. Simple-sequence repeat markers tightly linked to this QTL were identified for potential use in marker-assisted selection.     

Genetic mapping of quantitative trait loci affecting susceptibility to Marek's disease virus induced tumors in F2 intercross chickens.

Marek''s disease (MD) is a lymphoproliferative disease caused by the MD virus (MDV), which costs the poultry industry nearly $1 billion annually. To identify quantitative trait loci (QTL) affecting MD susceptibility, the inbred lines 6(3) (MD resistant) and 7(2) (MD susceptible) were mated to create more than 300 F2 chickens. The F2 chickens were challenged with MDV JM strain, moderately virulent) at 1 wk of age and assessed for MD susceptibility. The QTL analysis was divided into three stages. In stage 1, 65 DNA markers selected from the chicken genetic maps were typed on the 40 most MD-susceptible and the 40 most MD-resistant F2 chickens, and 21 markers residing near suggestive QTL were revealed by analysis of variance (ANOVA). In stage 2, the suggestive markers plus available flanking markers were typed on 272 F2 chickens, and three suggestive QTL were identified by ANOVA. In stage 3, using the interval mapping program Map Manager and permutation tests, two significant and two suggestive MD QTL were identified on four chromosomal subregions. Three to five loci collected explained between 11 and 23% of the phenotypic MD variation, or 32-68% of the genetic variance. This study constitutes the first report in the domestic chicken on the mapping of non-major histocompatibility complex QTL affecting MD susceptibility.     

QTL mapping analysis of plant height and ear height of maize (Zea mays L.)

Genetic map containing 103 microsatellite loci obtained on 200 F2 plants derived from the cross R15 x 478 was used for quantitative trait loci (QTL) mapping in maize. QTL were characterized in a population of 200 F2:4 lines, derived from selfing the F2 plants, and were evaluated with two replications in two environments. QTL determinations were made from the mean of these two environments. Plant height (PH) and ear height (EH) were measured. Using composite interval mapping (CIM) method, a total of 14 distinct QTLs were identified: nine for PH and five for EH. Additive, partial dominance, dominance, and overdominance actions existed among all detected QTL affecting plant height and ear height. The QTL explained 78.27% of the phenotypic variance of PH and 41.50% of EH. The 14 QTLs displayed mostly dominance or partial dominance gene action and mapped to chromosomes 2, 3, 4, 8 and 9.     

Teosinte Branched1 and the Origin of Maize: Evidence for Epistasis and the Evolution of Dominance

Two quantitative trait loci (QTL) controlling differences in plant and inflorescence architecture between maize and its progenitor (teosinte) were analyzed. Complementation tests indicate that one of these, which is on chromosome arm 1L, is the locus for the maize mutant teosinte branched1 (tb1). This QTL has effects on inflorescence sex and the number and length of internodes in the lateral branches and inflorescences. This QTL has strong phenotypic effects in teosinte background but reduced effects in maize background. The second QTL, which is on chromosome arm 3L, affects the same traits as the QTL on 1L. We identify two candidate loci for this QTL. The effects of this QTL on several traits are reduced in both maize and teosinte background as compared to a maize-teosinte F(2) population. Genetic background appears to affect gene action for both QTL. Analysis of a population in which both QTL were segregating revealed that they interact epistatically. Together, these two QTL substantially transform both plant and inflorescence architecture. We propose that tb1 is involved in the teosinte plant's response to local environment to produce either long or short branches and that maize evolution involved a change at this locus to produce short branches under all environments.