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.

No abstract

Black shank, caused by Phytophthora nicotianae, is typically the most important disease affecting tobacco (Nicotiana tabacum L.) production in the United States. Pedigree information suggests that most black shank resistance was derived from the cigar tobacco cultivar Florida 301. This resistance is thought to be polygenic in nature. The objectives of the current experiment were to (i) evaluate lines from a recombinant inbred line population derived from a cross between Florida 301 and the black shank‐susceptible cultivar Hicks for partial resistance using replicated field and greenhouse testing, (ii) genotype the population and use quantitative trait loci (QTL) analyses to identify Florida 301 genomic regions associated with resistance, and (iii) compare results with those obtained from a previous QTL analysis of a population derived from a cross involving ‘Beinhart 1000’. A total of 11 QTL affecting area under the disease progress curve were identified in both the field and greenhouse experiments. The QTL with the largest effect explained 16.9 and 18.6% of the phenotypic variation in the field and greenhouse experiments, respectively. This QTL was also found to have the largest effect on resistance in a Beinhart 1000 × Hicks doubled haploid mapping population. A major QTL found to affect resistance on linkage group 15 in the latter population, however, was not found to be important in the current population. Quantitative trait loci identification using greenhouse data was comparable to, if not superior to, use of field data.

cis-Abienol and sucrose esters are Nicotiana tabacum leaf surface components that likely influence plant resistance to pests. Their breakdown products also contribute to flavor and aroma characteristics of certain tobacco types. Mapping of genes involved in the biosynthesis of these compounds could permit development of molecular-based tools for generating tobacco types with novel cured leaf chemistry profiles. A doubled haploid mapping population segregating for major genes (Abl and BMVSE) affecting the ability to accumulate cis-abienol and sucrose esters was generated and genotyped with a large set of microsatellite markers. The two genes were found to reside on chromosome A of the N. tabacum genome with a distance of 8.2 cM (centimorgans) between them. Seventeen microsatellite markers were also placed on this linkage group, several of which exhibited complete cosegregation with Abl and BMVSE. Results should aid breeding efforts focused on modification of this aspect of tobacco cured leaf chemistry.

Multiple races of Phytophthora nicotianae (van Breda de Haan) cause the black shank disease of tobacco {NIcotiana tabacum L.). Identification of novel alíeles affecting resistance and associated DNA markers might help increase the range and level of cultivar resistance. A doubled haploid mapping population generated from a highly resistant x susceptible cross ('Beinhart 1000' x 'Hicks') was evaluated for resistance after inoculation with either race 0 or race 1 in a growth chamber and also genotyped at 206 microsatellite marker loci. Multiple interval mapping identified two major genomic regions affecting resistance to both races. A quantitative trait locus (QTL) on linkage group 8 explained 54.7 and 45.5% of the observed variation for end percent survival after race 0 and race 1 inoculation, respectively. A QTL on linkage group 4 explained a larger proportion (16.8%) of phenotypic variation for race 1 resistance as compared to race 0 resistance (1.8%). In combination with previously reported field data, the study authenticates the role of these two regions on black shank resistance. Correlations of line performance under field and growth chamber environments were good, and agreement was excellent at extreme levels of resistance or susceptibility. With appropriate isolate selection, growth chamber inoculations may provide a superior alternative to field evaluations for mapping QTL affecting black shank resistance. Identified QTL and associated markers may be useful for increasing levels of resistance to P. nicotianae in tobacco cultivars.