Prof. Dr. E. Bornberg-Bauer
Network evolution
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.
An
important finding is also that different families seem to have evolved according to different scenarios and that corresponding, alternative concepts need to be considered
when large scale properties of networks are being modeled. For example, for the bZIP proteins there were probably no major domain rearrangements involved and
the main force for shaping the network topology were presumably large scale duplications.
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