Genomic Signature of Complex Morphological Traits

Mimetic butterflies are an intriguing study object for evolutionary biology, because unrelated lineages have acquired very similar appearances to match their chemically defended models. The Mocker Swallowtail Papilio dardanus, a large butterfly widely distributed in subsaharan Africa, is a particularly striking example, because it expresses different morphological forms that each mimic a different model. From breeding studies it is well known that a single genetic locus controls the expression of different morphs. Here we aim to understand how this control functions on a molecular level, following up on older proposals that the complexity of diversity is likely to be controlled by equally complex genetic mechanisms, sometimes labelled as 'supergenes'. Starting with a 'candidate gene' that we recently discovered (coding for the transcription factor invected), we can now test the variation on the molecular level and its association with a diversity of mimetic colour morphs. DNA sequencing will reveal differences at single nucleotides (so-called SNPs) over a large region (some 200,000 base pairs), expected to differ in hundreds, if not thousands, of nucleotides in a morphologically variable population of P. dardanus. This will be the currency of various tests for sites under positive selection (as opposed to 'neutral' changes) presumably controlling the adaptively favourable phenotypes. Equally, 'hitch-hiking' of neutral sites with these functional sites under selection will affect larger portions of the genome, leaving a unique signature of selection. Identifying these functional sites will not only reveal the mechanism of how a gene can regulate the morphological variation, but also establishes the architecture of a complex locus on a molecular level, testing intriguing hypotheses from classical genetics. In addition, the method will demonstrate a more widely applicable approach on how to associate differences between living organisms and the genes producing these differences that are equally applicable to, for example, human disease genes showing advantageous variants in a population.