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Genotype, environment, and genotype by environment interactions determine quantitative resistance to leaf rust (Coleosporium asterum) in Euthamia graminifolia (Asteraceae)
Article first published online: 26 APR 2004
DOI: 10.1111/j.1469-8137.2004.01082.x
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How to Cite
Price, J. S., Bever, J. D. and Clay, K. (2004), Genotype, environment, and genotype by environment interactions determine quantitative resistance to leaf rust (Coleosporium asterum) in Euthamia graminifolia (Asteraceae). New Phytologist, 162: 729–743. doi: 10.1111/j.1469-8137.2004.01082.x
Publication History
- Issue published online: 26 APR 2004
- Article first published online: 26 APR 2004
- Received: 14 October 2003 Accepted: 16 January 2004; doi: 10.1111/j.1469-8137.2004.01082.x
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Keywords:
- clonal plant;
- environmental variation;
- fungal pathogen;
- genotypic basis;
- logistic analysis;
- quantitative disease resistance;
- Euthamia graminifolia (=Solidago graminifolia (Goldenrod));
- Coleosporium asterum
Summary
- • The strength and consistency of genotypic differences in disease resistance determine the potential for resistance evolution in host populations that rely on vegetative reproduction. Here we surveyed infection intensity of host genotypes across space and time to estimate genotypic and environmental effects on quantitative disease resistance.
- • Cloned fragments of 12 Euthamia graminifolia genotypes were grown in unweeded experimental fields and outdoor pots. Infection intensity was surveyed during 2 yr of natural infection by the non-systemic rust pathogen, Coleosporium asterum.
- • Five of six surveys detected infection intensity differences among genotypes, despite substantial variation in mean infection intensity across surveys. When resistance was defined relative to local pathogen density, 10–40% of resistance variation was due to host genotype. Although two genotypes exhibited greater resistance across environments, G × E interactions in resistance were common. Furthermore, infection intensity was unrelated to host size.
- • We conclude that quantitative resistance level can evolve in this system and show how logistic analysis (relative to local pathogen density) can provide insight into the mechanism(s) responsible for G × E interactions in infection intensity.