Title: "Dissecting Quantitative Disease Resistance: from QTL Mapping to Global Gene Expression Analysis"
Speaker: Dr. Dina St. Clair, Department of Vegetable Crops, University California, Davis
Place: Stanley Coulter (SC) 239; Tuesday, 4:30pm


Genetic inheritance of disease resistance in plants can be classified into two types: qualitative and quantitative. Unlike qualitative disease resistance, quantitative resistance in a segregating population typically displays a continuous phenotypic distribution controlled by multiple loci that may also interact with the environment and exhibit low heritability. Loci controlling quantitative resistance (resistance QTLs) are much less understood than qualitative 'R' genes in terms of their mechanism(s) of interaction with pathogens, how they interact to confer resistance, and how they 'fit' into gene pathways. However, quantitative resistance is an important means of genetic control of pathogens and deserves further study to better understand its genetic and molecular basis.

Our study of quantitative disease resistance uses a combination of quantitative genetics, statistics, molecular genetics and functional genomics in two species, tomato (Lycopersicon esculentum) and Arabidopsis thaliana. Our goals include the detailed characterization of structural and regulatory loci controlling quantitative resistance, and determination of how loci interact in pathways to produce the resistant phenotype.

In tomato, we are using a 'top-down' approach: QTL mapping in a population segregating for quantitative resistance to Phytophthora infestans, analysis of QTL-QTL interactions, and fine-mapping of QTLs in sub-near-isogenic lines. Next steps include high-resolution QTL mapping and map-based cloning of structural (and possibly regulatory) loci. In Arabidopsis, we are taking a 'bottom-up' approach to quantitative resistance because of the availability of a fully-sequenced, annotated genome and 'whole-genome' microarrays. We used whole-genome arrays to identify accessions that exhibit putative expression-level polymorphisms (ELPs) among loci that respond to induction by salicylic (SA) and jasmonic acid (JA), which induce expression of genes involved in disease resistance response pathways. Subsequently, we are genotyping a recombinant inbred line population derived from two accessions and subjecting it to microarray analysis. Global gene expression data will be used in two ways: DNA sequence information associated with each 'address' on the array that exhibits an SA- or JA-related ELP will be examined to identify loci involved in the response pathway, and QTL analysis will identify chromosomal regions associated with structural and regulatory loci. Results from both analyses will be compared to determine which regions likely contain candidate regulatory loci; several will be targeted for cloning and further characterization.