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First published online December 14, 2007; 10.1105/tpc.107.053827

The Plant Cell 19:4046-4060 (2007)
© 2007 American Society of Plant Biologists

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Natural Variation in RPS2-Mediated Resistance among Arabidopsis Accessions: Correlation between Gene Expression Profiles and Phenotypic Responses[W]

Remco M.P. Van Poeckea,1, Masanao Satoa,b, Lisa Lenarz-Wyatta, Sanford Weisbergc and Fumiaki Katagiria,2

a Department of Plant Biology, Microbial and Plant Genomics Institute, University of Minnesota, St. Paul, Minnesota 55108
b Department of Life Sciences, Graduate School of Arts and Sciences, University of Tokyo, Meguro-ku, Tokyo 153-8902, Japan
c School of Statistics, University of Minnesota, Minneapolis, Minnesota 55455

2 Address correspondence to katagiri{at}umn.edu.

Natural variation in gene expression (expression traits or e-traits) is increasingly used for the discovery of genes controlling traits. An important question is whether a particular e-trait is correlated with a phenotypic trait. Here, we examined the correlations between phenotypic traits and e-traits among 10 Arabidopsis thaliana accessions. We studied defense against Pseudomonas syringae pv tomato DC3000 (Pst), with a focus on resistance gene–mediated resistance triggered by the type III effector protein AvrRpt2. As phenotypic traits, we measured growth of the bacteria and extent of the hypersensitive response (HR) as measured by electrolyte leakage. Genetic variation among accessions affected growth of Pst both with (Pst avrRpt2) and without (Pst) the AvrRpt2 effector. Variation in HR was not correlated with variation in bacterial growth. We also collected gene expression profiles 6 h after mock and Pst avrRpt2 inoculation using a custom microarray. Clusters of genes whose expression levels are correlated with bacterial growth or electrolyte leakage were identified. Thus, we demonstrated that variation in gene expression profiles of Arabidopsis accessions collected at one time point under one experimental condition has the power to explain variation in phenotypic responses to pathogen attack.







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