We find ubiquitous compensatory mutations within functional sites, such that the energy phenotype and the function of a site evolve in a significantly more constrained way than does its sequence.
We also find evidence for substantial evolution of regulatory function involving point mutations as well as sequence insertions and deletions within binding sites.
Genes lose their regulatory link to a given transcription factor at a rate similar to the neutral point mutation rate, from which we infer a moderate average fitness advantage of functional over nonfunctional sites.
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We present a genomewide cross-species analysis of regulation for broad-acting transcription factors in yeast.
Our model for binding site evolution is founded on biophysics: the binding energy between transcription factor and site is a quantitative phenotype of regulatory function, and selection is given by a fitness landscape that depends on this phenotype.The model quantifies conservation, as well as loss and gain, of functional binding sites in a coherent way.Its predictions are supported by direct cross-species comparison between four yeast species., which possesses a remarkable range of stylar conditions and diverse types of floral morphology and pollination biology.Reconstruction of evolutionary change was complicated by incomplete resolution of trees inferred from two rapidly evolving chloroplast regions, but we bracketed reconstructions expected on the fully resolved plastid-based tree by considering all possible resolutions of polytomies on the shortest trees.Stigma-height dimorphism likely arose on several occasions in , respectively, are clearly not homologous, an evolutionary convergence unique to Amaryllidaceae.