The limited population sizes used in many quantitative trait locus (QTL) detection experiments can lead to underestimation of QTL number, overestimation of QTL effects, and failure to quantify QTL interactions. We used the barley/barley stripe rust pathosystem to evaluate the effect of population size on the estimation of QTL parameters. We generated a large (n = 409) population of doubled haploid lines derived from the cross of two inbred lines, BCD47 and Baronesse. This population was evaluated for barley stripe rust severity in the Toluca Valley, Mexico, and in Washington State, USA, under field conditions. BCD47 was the principal donor of resistance QTL alleles, but the susceptible parent also contributed some resistance alleles. The major QTL, located on the long arm of chromosome 4H, close to the Mlo gene, accounted for up to 34% of the phenotypic variance. Subpopulations of different sizes were generated using three methods-resampling, selective genotyping, and selective phenotyping-to evaluate the effect of population size on the estimation of QTL parameters. In all cases, the number of QTL detected increased with population size. QTL with large effects were detected even in small populations, but QTL with small effects were detected only by increasing population size. Selective genotyping and/or selective phenotyping approaches could be effective strategies for reducing the costs associated with conducting QTL analysis in large populations. The method of choice will depend on the relative costs of genotyping versus phenotyping.

The identification and location of sources of genetic resistance to plant diseases are important contributions to the development of resistant varieties. The combination of different sources and types of resistance in the same genotype should assist in the development of durably resistant varieties. Using a doubled haploid (DH), mapping population of barley, we mapped a qualitative resistance gene ( Rpsx) to barley stripe rust in the accession CI10587 (PI 243183) to the long arm of chromosome 1(7H). We combined the Rpsx gene, through a series of crosses, with three mapped and validated barley stripe rust resistance QTL alleles located on chromosomes 4(4H) (QTL4), 5(1H) (QTL5), and 7(5H) (QTL7). Three different barley DH populations were developed from these crosses, two combining Rpsx with QTL4 and QTL7, and the third combining Rpsx with QTL5. Disease severity testing in four environments and QTL mapping analyses confirmed the effects and locations of Rpsx, QTL4, and QTL5, thereby validating the original estimates of QTL location and effect. QTL alleles on chromosomes 4(4H) and 5(1H) were effective in decreasing disease severity in the absence of the resistance allele at Rpsx. Quantitative resistance effects were mainly additive, although magnitude interactions were detected. Our results indicate that combining qualitative and quantitative resistance in the same genotype is feasible. However, the durability of such resistance pyramids will require challenge from virulent isolates, which currently are not reported in North America.

Quantitative resistance (QR) to disease is usually more durable than qualitative resistance, but its genetic basis is not well understood. We used the barley/barley stripe rust pathosystem as a model for the characterization of the QR phenotype and associated genomic regions. As an intermediate step in the preparation of near-isogenic lines representing individual QTL alleles and combinations of QTL alleles in a homogeneous genetic background, we developed a set of QTL introgression lines in a susceptible background. These intermediate barley near-isogenic (i-BISON) lines represent disease resistance QTL combined in one-, two-, and three-way combinations in a susceptible background. We measured four components of disease resistance on the i-BISON lines: latent period, infection efficiency, lesion size, and pustule density. The greatest differences between the target QTL introgressions and the susceptible controls were for the latter three traits. On average, however, the QTL introgressions also had longer latent periods than the susceptible parent (Baronesse). There were significant differences in the magnitudes of effects of different QTL alleles. The 4H QTL allele had the largest effect, followed by the alleles on 1H and 5H. Pyramiding multiple QTL alleles led to higher levels of resistance in terms of all components of QR except latent period.

The beet-cyst nematode (Heterodera schachtii\ud Schmidt) is one of the major pests of sugar beet. The identification\ud of molecular markers associated with nematode tolerance\ud would be helpful for developing tolerant varieties. The\ud aim of this study was to identify single nucleotide polymorphism\ud (SNP) markers linked to nematode tolerance from the\ud Beta vulgaris ssp. maritima source WB242. A WB242-\ud derived F2 population was phenotyped for host-plant nematode\ud reaction revealing a 3:1 segregation ratio of the tolerant and\ud susceptible phenotypes and suggesting the action of a gene\ud designated as HsBvm-1. Bulked segregant analysis (BSA)\ud was used. The most tolerant and susceptible individuals were\ud pooled and subjected to restriction site associated DNA sequencing\ud (RAD-Seq) analysis, which identified 7,241 SNPs.\ud A subset of 384 candidate SNPs segregating between bulks\ud were genotyped on the 20 most-tolerant and most-susceptible\ud individuals, identifying a single marker (SNP192) showing\ud complete association with nematode tolerance. Segregation of\ud SNP192 confirmed the inheritance of tolerance by a single\ud gene. This association was further validated on a set of 26\ud commercial tolerant and susceptible varieties, showing the\ud presence of the SNP192 WB242-type allele only in the tolerant\ud varieties. We identified and mapped on chromosome 5 the first\ud nematode tolerance gene (HsBvm-1) from Beta vulgaris ssp.\ud maritima and released information on SNP192, a linked marker\ud valuable for high-throughput, marker-assisted breeding of nematode\ud tolerance in sugar beet

The use of molecular and quantitative trait locus (QTL) analysis tools initially lent support to the idea that relatively few genetic factors were the principal determinants of complex traits, including quantitative resistance (QR) to plant diseases. However, there are concerns regarding bias in QTL estimation and reproducibility of QTL effects in different genetic backgrounds. We are interested in mapping determinants of QR, and pyramiding resistance alleles at QTL loci may lead to durable resistance as well as provide independent validation of QTL effects and estimation of QTL interactions. We used molecular marker information to validate effects of resistance alleles at three QTL conferring QR to barley stripe rust (caused by Puccinia striiformis West. f. sp. hordei). Two of the QTL [one on chromosome 4(4H) and one on chromosome 7(5H)] trace to one parent, while another QTL on chromosome 5(1H) traces to a different parent. The pyramids of these QR alleles provide independent estimates of QTL effects, influence of genetic background on QTL effects, QTL × QTL interaction, and QTL × environment interaction. Our results validate QTL effect estimates, showing that a small number of QTL explained 94% of the genetic variation in trait expression in a new genetic background. Original QTL estimates were quantitatively biased, but that did not preclude the achievement of selection responses. We also confirmed the additive effects of the QTL alleles, as well as the consistent effects of QTL alleles across environments.

A set of barley (Hordeum vulgare L.) near-isogenic BISON (Barley stripe rust resistance ISOgeNic) lines was derived via the introgression of alleles conferring resistance to barley stripe rust (BSR; caused by Puccinia striiformis f. sp. hordei). The BISON lines represent all possible single and combinatorial allele introgressions at BSR resistance QTL on chromosomes 1H, 4H, and 5H. They are the result of more t han 20 y r of BSR resistance QT L mapping, charac ter izat ion,

Fields infested with sugarbeet cyst nematode (SBCN; Heterodera schachtii Schmidt) are common throughout the western United States and most of the world where sugarbeet (Beta vulgaris L.) is grown. Sugarbeet cyst nematode is potentially very devastating to sugarbeet production. The sugarbeet germplasms CN12‐446 (Reg. No. GP‐280, PI 657939), CN12‐770 (Reg. No. GP‐281, PI 657940), and CN72‐652 (Reg. No. GP‐279, PI 657938) have high levels of SBCN resistance and were developed and released by the USDA‐ARS at Salinas, CA in cooperation with the Beet Sugar Development Foundation in Denver, CO. CN12‐446, CN12‐770, and CN72‐652 are multigerm (MM), green hypocotyl (rr), and self‐fertile (Sf) lines that segregate for genetic male sterility (A‐: aa). They are S3 lines selected from two male‐sterile‐facilitated, random‐mated populations: CN12 and CN72. CN12‐446 and CN12‐770 are sister S2 lines and are more than 75% identical. Each is resistant to SBCN and powdery mildew (PM; caused by Erysiphe polygoni DC [syn. E. betae (Vanha) Weltzien]) and contains the Rz1 gene for resistance to Beet necrotic yellow vein virus, the causal agent of rhizomania. CN72‐652 is susceptible to rhizomania and PM. It is unknown if CN72‐652 has the same gene for SBCN resistance as CN12‐446 and CN12‐770.

Sugar beet (Beta vulgaris L.) genetic stock lines FC308 (PI701378) and FC309 (PI700990) are two highly homozygous and phenotypically homogenous sources of resistance to two sugar beet pests. FC308 is resistant to sugar beet cyst nematode (Heterodera schachtii), but susceptible to Fusarium yellows, while FC309 is Fusarium yellows resistant, but sugar beet cyst nematode susceptible. These two populations were developed by the USDA-ARS in Fort Collins, CO, derived from unreleased USDA-ARS Salinas germplasm lines. Multiple field and greenhouse trials for Fusarium yellows and nematode resistance confirmed the uniform phenotypes of both lines for each disease. To enable molecular breeders to rapidly screen proprietary markers in silico, gene space assemblies for each line were also developed. Genome sequencing of individual plants from each line, as well as pooled sequencing of sub-populations of both lines indicated fixation of a previously reported genetic variant linked to sugar beet cyst nematode resistance in FC308. However, two previously reported variants linked to Fusarium resistance appear to be unlinked to the resistance found in FC309. Collectively, these two new genetic stocks should prove useful as sources of resistance to Fusarium yellows and sugar beet cyst nematode, as model genetic backgrounds for studying plant-pathogen interactions, and for mapping the resistance genes present in these lines.