ArticlePLoS computational biology2010
Redundancy and the evolution of cis-regulatory element multiplicity.
Article in PLoS computational biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
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- Dual Eigen-modules of Cis-Element Regulation Profiles and Selection of Cognition-Language Eigen-direction along Evolution in Hominidae.Molecular biology and evolution · 2020Article
- Making sense of transcription networks.Cell · 2015Review
- Mechanisms of mutational robustness in transcriptional regulation.Frontiers in genetics · 2015Review
- Spurious transcription factor binding: non-functional or genetically redundant?BioEssays : news and reviews in molecular, cellular and developmental biology · 2014Article
- The evolution of complex gene regulation by low-specificity binding sites.Proceedings. Biological sciences · 2013Article
- The underlying molecular and network level mechanisms in the evolution of robustness in gene regulatory networks.PLoS computational biology · 2013Article
- Escape from Adaptive Conflict follows from weak functional trade-offs and mutational robustness.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Coevolution within and between regulatory loci can preserve promoter function despite evolutionary rate acceleration.PLoS genetics · 2012Article
- ncDNA and drift drive binding site accumulation.BMC evolutionary biology · 2012Article
- Evolutionary origins of transcription factor binding site clusters.Molecular biology and evolution · 2012Article
- Shadow enhancers: frequently asked questions about distributed cis-regulatory information and enhancer redundancy.BioEssays : news and reviews in molecular, cellular and developmental biology · 2012Article
- Evidence for directed evolution of larger size motif in Arabidopsis thaliana genome.TheScientificWorldJournal · 2012Article
- Adult Drosophila melanogaster evolved for antibacterial defense invest in infection-induced expression of both humoral and cellular immunity genes.BMC research notes · 2011Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The promoter regions of many genes contain multiple binding sites for the same transcription factor (TF). One possibility is that this multiplicity evolved through transitional forms showing redundant cis-regulation. To evaluate this hypothesis, we must disentangle the relative contributions of different evolutionary mechanisms to the evolution of binding site multiplicity. Here, we attempt to do this using a model of binding site evolution. Our model considers binding sequences and their interactions with TFs explicitly, and allows us to cast the evolution of gene networks into a neutral network framework. We then test some of the model's predictions using data from yeast. Analysis of the model suggested three candidate nonadaptive processes favoring the evolution of cis-regulatory element redundancy and multiplicity: neutral evolution in long promoters, recombination and TF promiscuity. We find that recombination rate is positively associated with binding site multiplicity in yeast. Our model also indicated that weak direct selection for multiplicity (partial redundancy) can play a major role in organisms with large populations. Our data suggest that selection for changes in gene expression level may have contributed to the evolution of multiple binding sites in yeast. We conclude that the evolution of cis-regulatory element redundancy and multiplicity is impacted by many aspects of the biology of an organism: both adaptive and nonadaptive processes, both changes in cis to binding sites and in trans to the TFs that interact with them, both the functional setting of the promoter and the population genetic context of the individuals carrying them.
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