Mutational Signatures in Wild Type Escherichia coli Strains Reveal Predominance of DNA Polymerase Errors.
Autor: | Garushyants SK; A.A. Kharkevich Institute for Information Transmission Problems, RAS, Moscow, Russia., Sane M; National Centre for Biological Sciences, Bengaluru, India., Selifanova MV; Faculty of Bioengineering and Bioinformatics, M.V. Lomonosov Moscow State University, Moscow, Russia., Agashe D; National Centre for Biological Sciences, Bengaluru, India., Bazykin GA; A.A. Kharkevich Institute for Information Transmission Problems, RAS, Moscow, Russia., Gelfand MS; A.A. Kharkevich Institute for Information Transmission Problems, RAS, Moscow, Russia.; Center for Molecular and Cellular Biology, Skolkovo Institute of Science and Technology (Skoltech), Moscow, Russia. |
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Jazyk: | angličtina |
Zdroj: | Genome biology and evolution [Genome Biol Evol] 2024 Apr 02; Vol. 16 (4). |
DOI: | 10.1093/gbe/evae035 |
Abstrakt: | While mutational processes operating in the Escherichia coli genome have been revealed by multiple laboratory experiments, the contribution of these processes to accumulation of bacterial polymorphism and evolution in natural environments is unknown. To address this question, we reconstruct signatures of distinct mutational processes from experimental data on E. coli hypermutators, and ask how these processes contribute to differences between naturally occurring E. coli strains. We show that both mutations accumulated in the course of evolution of wild-type strains in nature and in the lab-grown nonmutator laboratory strains are explained predominantly by the low fidelity of DNA polymerases II and III. By contrast, contributions specific to disruption of DNA repair systems cannot be detected, suggesting that temporary accelerations of mutagenesis associated with such disruptions are unimportant for within-species evolution. These observations demonstrate that accumulation of diversity in bacterial strains in nature is predominantly associated with errors of DNA polymerases. (© The Author(s) 2024. Published by Oxford University Press on behalf of Society for Molecular Biology and Evolution.) |
Databáze: | MEDLINE |
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