Author
Listed:
- Sinisa Bratulic
(University of Zurich
Swiss Institute of Bioinformatics, Quartier Sorge—Bâtiment Génopode)
- Macarena Toll-Riera
(University of Zurich
Swiss Institute of Bioinformatics, Quartier Sorge—Bâtiment Génopode)
- Andreas Wagner
(University of Zurich
Swiss Institute of Bioinformatics, Quartier Sorge—Bâtiment Génopode
The Santa Fe Institute)
Abstract
Phenotypic mutations are amino acid changes caused by mistranslation. How phenotypic mutations affect the adaptive evolution of new protein functions is unknown. Here we evolve the antibiotic resistance protein TEM-1 towards resistance on the antibiotic cefotaxime in an Escherichia coli strain with a high mistranslation rate. TEM-1 populations evolved in such strains endow host cells with a general growth advantage, not only on cefotaxime but also on several other antibiotics that ancestral TEM-1 had been unable to deactivate. High-throughput sequencing of TEM-1 populations shows that this advantage is associated with a lower incidence of weakly deleterious genotypic mutations. Our observations show that mistranslation is not just a source of noise that delays adaptive evolution. It could even facilitate adaptive evolution by exacerbating the effects of deleterious mutations and leading to their more efficient purging. The ubiquity of mistranslation and its effects render mistranslation an important factor in adaptive protein evolution.
Suggested Citation
Sinisa Bratulic & Macarena Toll-Riera & Andreas Wagner, 2017.
"Mistranslation can enhance fitness through purging of deleterious mutations,"
Nature Communications, Nature, vol. 8(1), pages 1-9, August.
Handle:
RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms15410
DOI: 10.1038/ncomms15410
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