Although the defensive and counter-defensive molecules underlying many ecological interactions are known, the genetic mechanisms controlling these molecules are often unknown. Knowledge of these mechanisms, as well as the selective forces and adaptations that have shaped them, is necessary if we are to understand the evolution of ecological interactions. In the thesis presented here the molecular mechanisms underlying two plantinsect interaction systems were investigated. Adaptive mutations allowing an insect to utilize a new food plant can have different molecular origins, affecting the regulatory regions as well as the coding sequence of genes. In general it is assumed that phase I and phase II enzymes are important in insects to detoxify plant allelochemicals, but detailed knowledge is still scarce. The first system involves the Pieridae butterflies and the Brassicaceae plants that have been in a coevolutionary arms race for about 80 million years. To circumvent the activated defense system of the plants, the Pieridae caterpillars posses a unique detoxifying enzyme called Nitrile-specifier protein (NSP), that redirects the hydrolysis of glucosinolates to less toxic nitriles rather than the toxic isothiocyanates in the caterpillar gut. Here the molecular origins of this novel detoxifying mechanism were investigated. It was found that NSP is a member of an insect specific gene family, called the NSP-like gene family. Members of this family consist of variable tandem repeats, are expressed in the gut lumen of the insect and are evolving in an ongoing birth-death process. NSP and its paralog MA evolved through two tandem duplications of the single domain gene SDMA in the Pieridae caterpillars that feed on glucosinolate containing plants. While gene duplication is a common mechanism to adapt to new environments, the molecular evolution of NSP provides a rare example of proven neofunctionalization after duplication. Future research on location, mode of action and genomic location of NSP are necessary to shed light on the mechanism of duplication and neofunctionalization that gave rise to NSP and MA.