title: Genome-wide association mapping in Arabidopsis identifies previously known flowering time and pathogen resistance genes.
abstract: There is currently tremendous interest in the possibility of using genome-wide association mapping to identify genes responsible for natural variation, particularly for human disease susceptibility. The model plant Arabidopsis thaliana is in many ways an ideal candidate for such studies, because it is a highly selfing hermaphrodite. As a result, the species largely exists as a collection of naturally occurring inbred lines, or accessions, which can be genotyped once and phenotyped repeatedly. Furthermore, linkage disequilibrium in such a species will be much more extensive than in a comparable outcrossing species. We tested the feasibility of genome-wide association mapping in A. thaliana by searching for associations with flowering time and pathogen resistance in a sample of 95 accessions for which genome-wide polymorphism data were available. In spite of an extremely high rate of false positives due to population structure, we were able to identify known major genes for all phenotypes tested, thus demonstrating the potential of genome-wide association mapping in A. thaliana and other species with similar patterns of variation. The rate of false positives differed strongly between traits, with more clinal traits showing the highest rate. However, the false positive rates were always substantial regardless of the trait, highlighting the necessity of an appropriate genomic control in association studies.
authors.affiliation: Molecular and Computational Biology, University of Southern California, Los Angeles, California, United States of America.
authors.forename: María José
authors.initials: MJ
authors.lastname: Aranzana
authors.forename: Sung
authors.initials: S
authors.lastname: Kim
authors.forename: Keyan
authors.initials: K
authors.lastname: Zhao
authors.forename: Erica
authors.initials: E
authors.lastname: Bakker
authors.forename: Matthew
authors.initials: M
authors.lastname: Horton
authors.forename: Katrin
authors.initials: K
authors.lastname: Jakob
authors.forename: Clare
authors.initials: C
authors.lastname: Lister
authors.forename: John
authors.initials: J
authors.lastname: Molitor
authors.forename: Chikako
authors.initials: C
authors.lastname: Shindo
authors.forename: Chunlao
authors.initials: C
authors.lastname: Tang
authors.forename: Christopher
authors.initials: C
authors.lastname: Toomajian
authors.forename: Brian
authors.initials: B
authors.lastname: Traw
authors.forename: Honggang
authors.initials: H
authors.lastname: Zheng
authors.forename: Joy
authors.initials: J
authors.lastname: Bergelson
authors.forename: Caroline
authors.initials: C
authors.lastname: Dean
authors.forename: Paul
authors.initials: P
authors.lastname: Marjoram
authors.forename: Magnus
authors.initials: M
authors.lastname: Nordborg
mesh_terms: D017360:Arabidopsis / Q000235:genetics*; D002874:Chromosome Mapping; D005189:False Positive Reactions; D017343:Genes, Plant; D020022:Genetic Predisposition to Disease; D014644:Genetic Variation; D018745:Genome, Plant; D005838:Genotype; D007113:Immunity, Innate; D015810:Linkage Disequilibrium