1. ¹School of Biological Sciences, University of Manchester, Stopford Building 3.614, Oxford Road, Manchester M13 9PT, UK
2. ²Department of Biology, Washington University, Campus Box 1137, St Louis, MO 63130-4899, USA
3. ³Department of Anatomy & Neurobiology, Washington University School of Medicine, 660 S Euclid Ave., St Louis, MO 63110, USA

Correspondence: PX Kover, School of Biological Sciences, University of Manchester, Stopford Building 3.614, Oxford Road, Manchester M13 9PT, UK. E-mail: kover@man.ac.uk

Received 3 September 2004; Accepted 12 January 2005; Published online 16 March 2005.

Abstract

Plant pathogens can severely reduce host yield and fitness. Thus, investigating the genetic basis of plant response to pathogens is important to further understand plant–pathogen coevolution and to improve crop production. The interaction between Arabidopsis thaliana and Pseudomonas syringae is an important model for studying the genetic basis of plant–pathogen interactions. Studies in this model have led to the discovery of many genes that differentiate a resistant from a susceptible plant. However, little is known about the genetic basis of quantitative variation in response to P. syringae. In this study, we investigate the genetic basis of three aspects of A. thaliana's response to P. syringae: symptom severity, bacterial population size and fruit production using a quantitative trait loci (QTL) analysis. We found two QTL for symptom severity and two for fruit production (possible candidate genes for observed QTL are discussed). We also found significant two-locus epistatic effect on symptom severity and fruit production. Although bacterial population size and symptom severity were strongly phenotypically correlated, we did not detect any QTL for bacterial population size. Despite the detected genetic variation observed for susceptibility, we found only a weak overall relationship between susceptibility traits and fitness, suggesting that these traits may not respond to selection.