Abstract:Tremendous progress has been made in recent years on developing statistical methods for mapping quantitative trait loci (QTL) from crosses of inbred lines. In this chapter, we provide an introduction of composite interval mapping and multiple interval mapping methods for mapping QTL from inbred line crosses and also detailed instructions to perform the analyses in Windows QTL Cartographer. For each method, we discuss the meaning of each option in the analysis procedures and how to understand and interpret the … Show more
“…The single/independent population QTL analysis was performed based on composite interval mapping (CIM) and implemented in the Windows QTL Cartographer software v2.5 [102]. Permutation tests set to an alpha-level of 0.05 were performed to determine population and trait specific LOD thresholds at aprroximately 3.0.…”
Much remains unknown of molecular events controlling the plant hypersensitive defense response (HR), a rapid localized cell death that limits pathogen spread and is mediated by resistance (R-) genes. Genetic control of the HR is hard to quantify due to its microscopic and rapid nature. Natural modifiers of the ectopic HR phenotype induced by an aberrant auto-active R-gene (Rp1-D21), were mapped in a population of 3,381 recombinant inbred lines from the maize nested association mapping population. Joint linkage analysis was conducted to identify 32 additive but no epistatic quantitative trait loci (QTL) using a linkage map based on more than 7000 single nucleotide polymorphisms (SNPs). Genome-wide association (GWA) analysis of 26.5 million SNPs was conducted after adjusting for background QTL. GWA identified associated SNPs that colocalized with 44 candidate genes. Thirty-six of these genes colocalized within 23 of the 32 QTL identified by joint linkage analysis. The candidate genes included genes predicted to be in involved programmed cell death, defense response, ubiquitination, redox homeostasis, autophagy, calcium signalling, lignin biosynthesis and cell wall modification. Twelve of the candidate genes showed significant differential expression between isogenic lines differing for the presence of Rp1-D21. Low but significant correlations between HR-related traits and several previously-measured disease resistance traits suggested that the genetic control of these traits was substantially, though not entirely, independent. This study provides the first system-wide analysis of natural variation that modulates the HR response in plants.
“…The single/independent population QTL analysis was performed based on composite interval mapping (CIM) and implemented in the Windows QTL Cartographer software v2.5 [102]. Permutation tests set to an alpha-level of 0.05 were performed to determine population and trait specific LOD thresholds at aprroximately 3.0.…”
Much remains unknown of molecular events controlling the plant hypersensitive defense response (HR), a rapid localized cell death that limits pathogen spread and is mediated by resistance (R-) genes. Genetic control of the HR is hard to quantify due to its microscopic and rapid nature. Natural modifiers of the ectopic HR phenotype induced by an aberrant auto-active R-gene (Rp1-D21), were mapped in a population of 3,381 recombinant inbred lines from the maize nested association mapping population. Joint linkage analysis was conducted to identify 32 additive but no epistatic quantitative trait loci (QTL) using a linkage map based on more than 7000 single nucleotide polymorphisms (SNPs). Genome-wide association (GWA) analysis of 26.5 million SNPs was conducted after adjusting for background QTL. GWA identified associated SNPs that colocalized with 44 candidate genes. Thirty-six of these genes colocalized within 23 of the 32 QTL identified by joint linkage analysis. The candidate genes included genes predicted to be in involved programmed cell death, defense response, ubiquitination, redox homeostasis, autophagy, calcium signalling, lignin biosynthesis and cell wall modification. Twelve of the candidate genes showed significant differential expression between isogenic lines differing for the presence of Rp1-D21. Low but significant correlations between HR-related traits and several previously-measured disease resistance traits suggested that the genetic control of these traits was substantially, though not entirely, independent. This study provides the first system-wide analysis of natural variation that modulates the HR response in plants.
“…For both populations, the QTL analyses were done individually per location and with the mean across environments to deduce balanced values for each RIL. Epistatic interaction analyses were performed with multiple interval mapping (MIM) in WinQTL Cartographer v.2.5 software using the option "Scan through QTL mapping results file" and later refined using the option "Testing for existing QTLs" under the AIC-based selection criteria (Wang et al 2007;Silva et al 2012). Window size was set at 5 cM for each dataset section using forward and backward stepwise regression.…”
Epistasis and genetic background were important influences on expression of stripe rust resistance in two wheat RIL populations, one with resistance conditioned by two major genes and the other conditioned by several minor QTL. Stripe rust is a foliar disease of wheat (Triticum aestivum L.) caused by the air-borne fungus Puccinia striiformis f. sp. tritici and is present in most regions around the world where commercial wheat is grown. Breeding for durable resistance to stripe rust continues to be a priority, but also is a challenge due to the complexity of interactions among resistance genes and to the wide diversity and continuous evolution of the pathogen races. The goal of this study was to detect chromosomal regions for resistance to stripe rust in two winter wheat populations, 'Tubbs'/'NSA-98-0995' (T/N) and 'Einstein'/'Tubbs' (E/T), evaluated across seven environments and mapped with diversity array technology and simple sequence repeat markers covering polymorphic regions of ≈1480 and 1117 cM, respectively. Analysis of variance for phenotypic data revealed significant (P < 0.01) genotypic differentiation for stripe rust among the recombinant inbred lines. Results for quantitative trait loci/locus (QTL) analysis in the E/T population indicated that two major QTL located in chromosomes 2AS and 6AL, with epistatic interaction between them, were responsible for the main phenotypic response. For the T/N population, eight QTL were identified, with those in chromosomes 2AL and 2BL accounting for the largest percentage of the phenotypic variance.
“…QTL analysis was performed using composite interval mapping (CIM) in WinQTL Cartographer v.2.5 (Wang et al 2007). Epistatic interactions analyses were performed with multiple interval mapping (MIM) in WinQTL Cartographer v.2.5 using the option "Scan through QTL mapping results file" and later refined using the option "Testing for existing QTLs" under the AIC-based selection criteria (Silva et al 2012;Wang et al 2007). Likelihood-odds (LOD) thresholds for declaring statistical significance were calculated by 1,000 permutations (Churchill and Doerge 1994).…”
Identification of genome regions linked to Cephalosporium stripe resistance across two populations on chromosome 3BS, 4BS, 5AL, C5BL. Results were compared to a similar previous study. Cephalosporium stripe is a vascular wilt disease of winter wheat (Triticum aestivum L.) caused by the soil-borne fungus Cephalosporium gramineum Nisikado & Ikata. In the USA it is known to be a recurring disease when susceptible cultivars are grown in the wheat-growing region of Midwest and Pacific Northwest. There is no complete resistance in commercial wheat cultivars, although the use of moderately resistant cultivars reduces the disease severity and the amount of inoculum in subsequent seasons. The goal of this study was to detect and to compare chromosomal regions for resistance to Cephalosporium stripe in two winter wheat populations. Field inoculation was performed and Cephalosporium stripe severity was visually scored as percent of prematurely ripening heads (whiteheads) per plot. 'Tubbs'/'NSA-98-0995' and 'Einstein'/'Tubbs', each comprising a cross of a resistant and a susceptible cultivar, with population sizes of 271 and 259 F (5:6) recombinant inbred lines, respectively, were genotyped and phenotyped across four environments. In the quantitative trait loci (QTL) analysis, six and nine QTL were found, explaining in total, around 30 and 50 % of the phenotypic variation in 'Tubbs'/'NSA-98-0995' and 'Einstein'/'Tubbs', respectively. The QTL with the largest effect from both 'NSA-98-0995' and 'Einstein' was on chromosome 5AL.1 and linked to marker gwm291. Several QTL with smaller effects were identified in both populations on chromosomes 5AL, 6BS, and 3BS, along with other QTL identified in just one population. These results indicate that resistance to Cephalosporium stripe in both mapping populations was of a quantitative nature.
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