Resistance Quantitative Loci Research Articles

A molecular linkage map of tomato displaying chromosomal locations of resistance gene analogs based on a Lycopersicon esculentum x Lycopersicon hirsutum cross.

A molecular linkage map of tomato was constructed based on a BC1 population (N = 145) of a cross between Lycopersicon esculentum Mill. line NC84173 (maternal and recurrent parent) and Lycopersicon hirsutum Humb. and Bonpl. accession PI126445. NC84173 is an advanced breeding line that is resistant to several tomato diseases, not including early blight (EB) and late blight (LB). PI126445 is a self-incompatible accession that is resistant to many tomato diseases, including EB and LB. The map included 142 restriction fragment length polymorphism (RFLP) markers and 29 resistance gene analogs (RGAs). RGA loci were identified by PCR amplification of genomic DNA from the BC1 population, using ten pairs of degenerate oligonucleotide primers designed based on conserved leucine-rich repeat (LRR), nucleotide binding site (NBS), and serine (threonine) protein kinase (PtoKin) domains of known resistance genes (R genes). The PCR-amplified DNAs were separated by denaturing polyacrylamide gel electrophoresis (PAGE), which allowed separation of heterogeneous products and identification and mapping of individual RGA loci. The map spanned 1469 cM of the 12 tomato chromosomes with an average marker distance of 8.6 cM. The RGA loci were mapped to 9 of the 12 tomato chromosomes. Locations of some RGAs coincided with locations of several known tomato R genes or quantitative resistance loci (QRLs), including Cf-1, Cf-4, Cf-9, Cf-ECP2, rx-1, and Cm1.1 (chromosome 1); Tm-1 (chromosome 2); Asc (chrromosme 3); Pto, Fen, and Prf (chromosome 5); 01-1, Mi, Ty-1, Cm6.1, Cf-2, CF-5, Bw-5, and Bw-1 (chromosome 6); I-1, 1-3, and Ph-1 (chromosome 7); Tm-2a and Fr1 (chromosome 9); and Lv (chromosome 12). These co-localizations indicate that the RGA loci were either linked to or part of the known R genes. Furthermore, similar to that for many R gene families, several RGA loci were found in clusters, suggesting their potential evolutionary relationship with R genes. Comparisons of the present map with other molecular linkage maps of tomato, including the high density L. esculentum x Lycopersicon pennellii map, indicated that the lengths of the maps and linear order of RFLP markers were in good agreement, though certain chromosomal regions were less consistent than others in terms of the frequency of recombination. The present map provides a basis for identification and mapping of genes and QTLs for disease resistance and other desirable traits in PI126445 and other L. hirsutum accessions, and will be useful for marker-assisted selection and map-based gene cloning in tomato.

Coincidence in map positions between pathogen-induced defense-responsive genes and quantitative resistance loci in rice

Quantitative disease resistance conferred by quantitative trait loci (QTLs) is presumably of wider spectrum and durable. Forty-four cDNA clones, representing 44 defense-responsive genes, were fine mapped to 56 loci distributed on 9 of the 12 rice chromosomes. The locations of 32 loci detected by 27 cDNA clones were associated with previously identified resistance QTLs for different rice diseases, including blast, bacterial blight, sheath blight and yellow mottle virus. The loci detected by the same multiple-copy cDNA clones were frequently located on similar locations of different chromosomes. Some of the multiple loci detected by the same clones were all associated with resistance QTLs. These results suggest that some of the genes may be important components in regulation of defense responses against pathogen invasion and they may be the candidates for studying the mechanism of quantitative disease resistance in rice.

Defense response genes co-localize with quantitative disease resistance loci in pepper

Functional bases of polygenically inherited disease resistance are still unknown. In recent years, molecular dissection of polygenic resistance has led to the identification and location of quantitative trait loci (QTLs) on many plant genetic linkage maps. This process is a pre-requisite for resistance QTL characterization at a molecular and functional level. Here, we report the use of a candidate gene approach based on the hypothesis that some resistance QTLs previously mapped in pepper may correspond to defense response (DR) genes. Degenerate oligonucleotide primers were designed for conserved regions of two DR gene families: pathogenesis-related proteins (PR) of class 2 (β-1,3-glucanase) and PR proteins of class 5 (antifungal activity). Cloned pepper PCR-products as well as other solanaceous DR gene families were used as RFLP probes for mapping in three intraspecific maps of the pepper genome. A total of 12 probes out of 23 were positioned and generated 16 loci. Some DR probes revealed multiple gene copies in the pepper genome (PR5, β-1,3-glucanase, chitinase and Glutathione S-transferase). Genes encoding acidic and basic β-1,3-glucanases were clustered on linkage group (LG) P1a, whereas genes encoding chitinases occurred on several LGs (P1b, P2a and P5). A class-III chitinase gene co-localized with a major-effect QTL controlling resistance to Phytophthora capsici on LG P5. PR4, PR2 and PR10 loci mapped within the region of resistance QTLs to P. capsici (LG P1b), Potato virus Y (LG P1a) and Potyvirus E (LG P3), respectively. A digenic interaction between a PR4 and a PR2 loci explained a large effect (35%) of the resistance to Potyvirus E.

Quantitative trait loci analysis of powdery mildew disease resistance in the Arabidopsis thaliana accession kashmir-1.

Powdery mildew diseases are economically important diseases, caused by obligate biotrophic fungi of the Erysiphales. To understand the complex inheritance of resistance to the powdery mildew disease in the model plant Arabidopsis thaliana, quantitative trait loci analysis was performed using a set of recombinant inbred lines derived from a cross between the resistant accession Kashmir-1 and the susceptible accession Columbia glabrous1. We identified and mapped three independent powdery mildew quantitative disease resistance loci, which act additively to confer disease resistance. The locus with the strongest effect on resistance was mapped to a 500-kbp interval on chromosome III.

Mapping quantitative and qualitative disease resistance genes in a doubled haploid population of barley (Hordeum vulgare)

Stripe rust, leaf rust, and Barley Yellow Dwarf Virus (BYDV) are important diseases of barley (Hordeum vulgare L). Using 94 doubled-haploid lines (DH) from the cross of Shyri x Galena, multiple disease phenotype datasets, and a 99-marker linkage map, we determined the number, genome location, and effects of genes conferring resistance to these diseases. We also mapped Resistance Gene Analog Polymorphism (RGAP) loci, based on degenerate motifs of cloned disease resistance genes, in the same population. Leaf rust resistance was determined by a single gene on chromosome 1 (7H). QTLs on chromosomes 2 (2H), 3 (3H), 5 (1H), and 6 (6H) were the principal determinants of resistance to stripe rust. Two- locus QTL interactions were significant determinants of resistance to this disease. Resistance to the MAV and PAV serotypes of BYDV was determined by coincident QTLs on chromosomes 1 (7H), 4 (4H), and 5 (1H). QTL interactions were not significant for BYDV resistance. The associations of molecular markers with qualitative and quantitative disease resistance loci will be a useful information for marker-assisted selection.

QTL mapping and quantitative disease resistance in plants.

Quantitative trait locus (QTL) mapping is a highly effective approach for studying genetically complex forms of plant disease resistance. With QTL mapping, the roles of specific resistance loci can be described, race-specificity of partial resistance genes can be assessed, and interactions between resistance genes, plant development, and the environment can be analyzed. Outstanding examples include: quantitative resistance to the rice blast fungus, late blight of potato, gray leaf spot of maize, bacterial wilt of tomato, and the soybean cyst nematode. These studies provide insights into the number of quantitative resistance loci involved in complex disease resistance, epistatic and environmental interactions, race-specificity of partial resistance loci, interactions between pathogen biology, plant development and biochemistry, and the relationship between qualitative and quantitative loci. QTL mapping also provides a framework for marker-assisted selection of complex disease resistance characters and the positional cloning of partial resistance genes.