ArticleGenome biology and evolution2020
Independent Transposon Exaptation Is a Widespread Mechanism of Redundant Enhancer Evolution in the Mammalian Genome.
Article in Genome biology and evolution, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Genome architecture shapes the evolutionary origins of redundant enhancers in fly and mouse.bioRxiv : the preprint server for biology · 2026Article
- Regulatory changes in the fatty acid elongase eloF underlie the evolution of sex-specific pheromone profiles in Drosophila prolongata.BMC biology · 2025Article
- Regulatory Changes in the Fatty Acid ElongasebioRxiv : the preprint server for biology · 2024Article
- Article
- Expression of Transposable Elements throughout theNon-coding RNA · 2024Article
- Review
- Transposons contribute to the acquisition of cell type-specific cis-elements in the brain.Communications biology · 2023Article
- Detecting Horizontal Transfer of Transposons.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Genome Stability Is in the Eye of the Beholder: CR1 Retrotransposon Activity Varies Significantly across Avian Diversity.Genome biology and evolution · 2021Article
- Enhancer redundancy in development and disease.Nature reviews. Genetics · 2021Review
- Mechanisms of enhancer action: the known and the unknown.Genome biology · 2021Review
- Genome sequencing of deep-sea hydrothermal vent snails reveals adaptions to extreme environments.GigaScience · 2020Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many regulatory networks appear to involve partially redundant enhancers. Traditionally, such enhancers have been hypothesized to originate mainly by sequence duplication. An alternative model postulates that they arise independently, through convergent evolution. This mechanism appears to be counterintuitive to natural selection: Redundant sequences are expected to either diverge and acquire new functions or accumulate mutations and become nonfunctional. Nevertheless, we show that at least 31% of the redundant enhancer pairs in the human genome (and 17% in the mouse genome) indeed originated in this manner. Specifically, for virtually all transposon-derived redundant enhancer pairs, both enhancer partners have evolved independently, from the exaptation of two different transposons. In addition to conferring robustness to the system, redundant enhancers could provide an evolutionary advantage by fine-tuning gene expression. Consistent with this hypothesis, we observed that the target genes of redundant enhancers exhibit higher expression levels and tissue specificity as compared with other genes. Finally, we found that although enhancer redundancy appears to be an intrinsic property of certain mammalian regulatory networks, the corresponding enhancers are largely species-specific. In other words, the redundancy in these networks is most likely a result of convergent evolution.
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