Abstract:
Flowering plants show a dazzling variety of floral morphologies. To a large extent, these reflect co-evolution between plants and their animals pollinators and serve to enhance outbreeding. One particularly fascinating adaptation is heterostyly, where individuals within one species either form flowers with short styles and long stamens, or with long styles and short stamens. These two forms (or morphs) are controlled by the S-locus supergene that comprises at least three, more likely five individual causal genes controlling the different traits that are held together in tight linkage by suppressed recombination. However, the identities of the component genes remain unknown. We have recently identified the Primula CYP734A50 gene, encoding a putative brassinosteroid-degrading enzyme, as the G locus that determines the style-length dimorphism, and I will discuss these findings in light of classical models about the genetic and evolutionary basis of heterostyly.
Under certain ecological scenarios, animal-mediated outbreeding tends to give way to selfing, and this transition is generally accompanied by a suite of morphological and functional changes to the flowers, termed the selfing syndrome. This includes for example a dramatic reduction in flower size and in scent production. We are using the pair of closely related species Capsella grandiflora and C. rubella to study the molecular basis of evolutionary changes in flower size. The outbreeding ancestor C. grandiflora forms large attractive flowers, while the derived selfing species C. rubella only shows small, inconspicuous flowers. Using a quantitative-genetic approach, we have identified three genes whose variation between the two species contributes to flower-size reduction in C. rubella. I will present our unpublished findings about one of these that highlights the importance of natural variation in splicing efficiency for phenotypic evolution.
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