Although polyploidy is believed to be a major source of evolutionary novelty, few studies have examined the genetic basis of phenotypic variation in wild polyploids. In this thesis I have studied the genetic basis of flowering time variation in the wild tetraploid crucifer Capsella bursa-pastoris, as well as the evolutionary history of this species. First, phylogenetic methods were employed to test hypotheses on the origin of C. bursa-pastoris. Based on DNA sequences from two chloroplast DNA loci and three independent nuclear genes, we found no support for the notion of C. bursa-pastoris as an autopolyploid of the diploid C. grandiflora, or an allopolyploid of C. grandiflora and C. rubella, even though some C. bursa-pastoris accessions shared alleles with C. rubella at nuclear loci. Using divergence population genetic methods, a larger sample of accessions and data for six duplicated nuclear genes, we found that allele sharing in sympatry was better explained by introgressive hybridization than by multiple origins of the tetraploid. The genetic basis of flowering time variation was examined using three approaches. A gene expression microarray study revealed that early- and late-flowering accessions differ in circadian rhythm, as well as in the gibberellin pathway affecting flowering time. Second, two QTL (Quantitative Trait Loci) for flowering time map to duplicated linkage groups. Third, polymorphisms at the candidate genes CRYPTOCHROME1 (CRY1), in one of the QTL regions, and FLOWERING LOCUS C (FLC) are associated with natural flowering time variation. Different FLC splice site polymorphisms are associated with flowering time in samples from Western Eurasia and China. The CRY1 association is only found in Europe, where alleles introgressed from C. rubella have an effect on flowering time. In conclusion, duplicated genes, introgressive hybridization and splicing variation may all have played a role in the evolution of flowering time variation in C. bursa-pastoris.