ArticleScience advances2016
Mutation at a distance caused by homopolymeric guanine repeats in Saccharomyces cerevisiae.
Article in Science advances, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Flight style and metabolism shape the tempo of genome evolution in birds.PLoS biology · 2026Article
- Quantifying cell divisions along evolutionary lineages in cancer.Nature genetics · 2025Article
- The putative error prone polymerasenpj antimicrobials and resistance · 2024Article
- A singular PpaA/AerR-like protein inmSystems · 2023Article
- Cellular Responses to Widespread DNA Replication Stress.International journal of molecular sciences · 2023Review
- GIGYF1 disruption associates with autism and impaired IGF-1R signaling.The Journal of clinical investigation · 2022Article
- Constraints and consequences of the emergence of amino acid repeats in eukaryotic proteins.Nature structural & molecular biology · 2017Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutation provides the raw material from which natural selection shapes adaptations. The rate at which new mutations arise is therefore a key factor that determines the tempo and mode of evolution. However, an accurate assessment of the mutation rate of a given organism is difficult because mutation rate varies on a fine scale within a genome. A central challenge of evolutionary genetics is to determine the underlying causes of this variation. In earlier work, we had shown that repeat sequences not only are prone to a high rate of expansion and contraction but also can cause an increase in mutation rate (on the order of kilobases) of the sequence surrounding the repeat. We perform experiments that show that simple guanine repeats 13 bp (base pairs) in length or longer (G 13+ ) increase the substitution rate 4- to 18-fold in the downstream DNA sequence, and this correlates with DNA replication timing (R = 0.89). We show that G 13+ mutagenicity results from the interplay of both error-prone translesion synthesis and homologous recombination repair pathways. The mutagenic repeats that we study have the potential to be exploited for the artificial elevation of mutation rate in systems biology and synthetic biology applications.
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