Joost J. B. Keurentjes,3
Olivier Le Gall,1
Frédéric Revers,1 and
1UMR Génomique, Diversité et Pouvoir Pathogène, Institut National de la Recherche Agronomique (INRA)-Université Bordeaux 2, IBVM, , BP81, 33883 Villenave d'Ornon, France; 2Station de Génétique et d'Amélioration des Plantes, INRA, route de Saint Cyr, 78026 Versailles cedex; France 3Laboratory of Plant Physiology and Genetics, Wageningen University, NL-6703 BD, Wageningen, The Netherlands
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Accepted 12 October 2007.
In compatible interactions between plants and viruses that result in systemic infection, symptom development is a major phenotypic trait. However, host determinants governing this trait are mostly unknown, and the mechanisms underlying it are still poorly understood. In a previous study on the Arabidopsis thaliana--Plum pox virus (PPV) pathosystem, we showed a large degree of variation in symptom development among susceptible accessions. In particular, Cvi-1 (Cape Verde islands) accumulates viral particules but remains symptomless, Col-0 (Columbia) sometimes shows weak symptoms compared with Ler (Landsberg erecta), which always shows severe symptoms. Genetic analyses of Col × Ler and Cvi × Ler F2 and recombinant inbred line (RIL) populations suggested that symptom development as well as viral accumulation traits are polygenic and quantitative. Three of the symptom quantitative trait loci (QTL) identified could be confirmed in near-isogenic lines, including PSI1 (PPV symptom induction 1), which was identified on the distal part of chromosome 1 in both RIL populations. With respect to viral accumulation, several factors have been detected and, interestingly, in the Col × Ler population, two out of three viral accumulation QTL colocalized with loci controlling symptom development, although correlation analysis showed weak linearity between symptom severity and virus accumulation. In addition, in the Cvi × Ler RIL population, a digenic recessive determinant controlling PPV infection was identified.
© 2008 The American Phytopathological Society