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Lookup NU author(s): Dr Sergey MelnikovORCiD
This is the authors' accepted manuscript of an article that has been published in its final definitive form by National Academy of Sciences, 2018.
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© 2018 National Academy of Sciences. All rights reserved.Intracellular organisms, such as obligate parasites and endosymbionts, typically possess small genomes due to continuous genome decay caused by an environment with alleviated natural selection. Previously, a few species with highly reduced genomes, including the intracellular pathogens Mycoplasma and Microsporidia, have been shown to carry degenerated editing domains in aminoacyl-tRNA synthetases. These defects in the protein synthesis machinery cause inaccurate translation of the genetic code, resulting in significant statistical errors in protein sequences that are thought to help parasites to escape immune response of a host. In this study we analyzed 10,423 complete bacterial genomes to assess conservation of the editing domains in tRNA synthetases, including LeuRS, IleRS, ValRS, ThrRS, AlaRS, and PheRS. We found that, while the editing domains remain intact in free-living species, they are degenerated in the overwhelming majority of host-restricted bacteria. Our work illustrates that massive genome erosion triggered by an intracellular lifestyle eradicates one of the most fundamental components of a living cell: the system responsible for proofreading of amino acid selection for protein synthesis. This finding suggests that inaccurate translation of the genetic code might be a general phenomenon among intercellular organisms with reduced genomes.
Author(s): Melnikov SV, van den Elzen A, Stevens DL, Thoreen CC, Soll D
Publication type: Article
Publication status: Published
Journal: Proceedings of the National Academy of Sciences of the United States of America
Year: 2018
Volume: 115
Issue: 49
Pages: E11505-E11512
Print publication date: 04/12/2018
Online publication date: 19/11/2018
Acceptance date: 18/10/2018
Date deposited: 16/07/2020
ISSN (print): 0027-8424
ISSN (electronic): 1091-6490
Publisher: National Academy of Sciences
URL: https://doi.org/10.1073/pnas.1815992115
DOI: 10.1073/pnas.1815992115
PubMed id: 30455292
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