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Título: | High fidelity deep sequencing reveals no effect of ATM, ATR, and DNA-PK cellular DNA damage response pathways on adenovirus mutation rate |
Autor: | Risso-Ballester, Jennifer; Sanjuán, Rafael CSIC ORCID | Palabras clave: | Mutation rate Human adenovirus type 5 DNA damage response Experimental evolution |
Fecha de publicación: | 2019 | Editor: | Multidisciplinary Digital Publishing Institute | Citación: | Viruses 11(10): 938 (2019) | Resumen: | Most DNA viruses exhibit relatively low rates of spontaneous mutation. However, the molecular mechanisms underlying DNA virus genetic stability remain unclear. In principle, mutation rates should not depend solely on polymerase fidelity, but also on factors such as DNA damage and repair efficiency. Most eukaryotic DNA viruses interact with the cellular DNA damage response (DDR), but the role of DDR pathways in preventing mutations in the virus has not been tested empirically. To address this goal, we serially transferred human adenovirus type 5 in cells in which the telangiectasia-mutated PI3K-related protein kinase (ATM), the ATM/Rad3-related (ATR) kinase, and the DNA-dependent protein kinase (DNA-PK) were chemically inactivated, as well as in control cells displaying normal DDR pathway functioning. High-fidelity deep sequencing of these viral populations revealed mutation frequencies in the order of one-millionth, with no detectable effect of the inactivation of DDR mediators ATM, ATR, and DNA-PK on adenovirus sequence variability. This suggests that these DDR pathways do not play a major role in determining adenovirus genetic diversity. | Descripción: | This article belongs to the Section Animal Viruses. | Versión del editor: | https://doi.org/10.3390/v11100938 | URI: | http://hdl.handle.net/10261/220687 | DOI: | 10.3390/v11100938 | E-ISSN: | 1999-4915 |
Aparece en las colecciones: | (I2SysBio) Artículos |
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