Explaining the evolution of complexity has been a challenge to Darwinian theory since its conception. At the molecular level, biological complexity involves networks of ligand-protein, protein-protein and protein-nucleic acid interactions in metabolism, signal transduction, gene regulation, protein synthesis and so on. The duplication of genes is the predominant mechanism for the generation of new members of a protein family and so is central to the evolution of complexity. The duplication that increases the size of a network may occur either via single-gene duplication events or by duplication of genes on a large-scale, including the entire genome. The need for networks to remain stable and functional in the cellular environment after the duplication event(s) is thought to favor whole-genome duplication By combining phylogenetic, proteomic and structural information, we have elucidated the evolutionary driving forces for the gene-regulatory interaction networks of bHLH transcription factors. We infer that recurrent events of single-gene duplication and domain rearrangement repeatedly gave rise to distinct networks with almost identical hub-based topologies, and multiple activators and repressors. We thus provide the first empirical evidence for: scale-free protein networks emerging through single-gene duplications, the dominant importance of molecular modularity in the bottom-up construction of complex biological entities, and the convergent evolution of networks.
References
[1] G. Amoutzias, D.L. Robertson, S.G. Oliver and E. Bornberg-Bauer, 2004, Convergent Evolution of Gene Networks by single-gene duplication in higher eukaryotes. EMBO Reports. 5:274-279.
[2] G. Amoutzias, D.L. Robertson and E. Bornberg-Bauer, 2004, Evolution of protein-protein interaction networks in homo- and heterodimerising eukaryotic transcription factors. Comparative and Functional Genomics. 5:79-84.
