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Hierarchy and feedback in the evolution of the Escherichia coli transcription network.

TitleHierarchy and feedback in the evolution of the Escherichia coli transcription network.
Publication TypeJournal Article
Year of Publication2007
AuthorsCosentino Lagomarsino, M, Jona, P, Bassetti, B, Isambert, H
JournalProc Natl Acad Sci U S A
Date Published2007 Mar 27
KeywordsBinding Sites, Data Interpretation, Statistical, DNA, Escherichia coli, Escherichia coli Proteins, Evolution, Molecular, Feedback, Physiological, Gene Expression Regulation, Bacterial, Gene Transfer, Horizontal, Models, Biological, Models, Genetic, Monte Carlo Method, Protein Structure, Tertiary, Transcription Factors, Transcription, Genetic

The Escherichia coli transcription network has an essentially feedforward structure, with abundant feedback at the level of self-regulations. Here, we investigate how these properties emerged during evolution. An assessment of the role of gene duplication based on protein domain architecture shows that (i) transcriptional autoregulators have mostly arisen through duplication, whereas (ii) the expected feedback loops stemming from their initial cross-regulation are strongly selected against. This requires a divergent coevolution of the transcription factor DNA-binding sites and their respective DNA cis-regulatory regions. Moreover, we find that the network tends to grow by expansion of the existing hierarchical layers of computation, rather than by addition of new layers. We also argue that rewiring of regulatory links due to mutation/selection of novel transcription factor/DNA binding interactions appears not to significantly affect the network global hierarchy, and that horizontally transferred genes are mainly added at the bottom, as new target nodes. These findings highlight the important evolutionary roles of both duplication and selective deletion of cross-talks between autoregulators in the emergence of the hierarchical transcription network of E. coli.

Alternate JournalProc. Natl. Acad. Sci. U.S.A.
PubMed ID17372223
PubMed Central IDPMC1838485