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- W2034979835 endingPage "564" @default.
- W2034979835 startingPage "551" @default.
- W2034979835 abstract "Copy number variation is a major source of variation between individuals that is increasingly recognized as influencing genome evolution and human disease. But how does it arise? The authors discuss predicted mechanisms of copy number change, including non-homologous end-joining and non-homologous repair of broken replication forks. Deletions and duplications of chromosomal segments (copy number variants, CNVs) are a major source of variation between individual humans and are an underlying factor in human evolution and in many diseases, including mental illness, developmental disorders and cancer. CNVs form at a faster rate than other types of mutation, and seem to do so by similar mechanisms in bacteria, yeast and humans. Here we review current models of the mechanisms that cause copy number variation. Non-homologous end-joining mechanisms are well known, but recent models focus on perturbation of DNA replication and replication of non-contiguous DNA segments. For example, cellular stress might induce repair of broken replication forks to switch from high-fidelity homologous recombination to non-homologous repair, thus promoting copy number change." @default.
- W2034979835 created "2016-06-24" @default.
- W2034979835 creator A5000612576 @default.
- W2034979835 creator A5026001356 @default.
- W2034979835 creator A5068732023 @default.
- W2034979835 creator A5078360141 @default.
- W2034979835 date "2009-08-01" @default.
- W2034979835 modified "2023-10-17" @default.
- W2034979835 title "Mechanisms of change in gene copy number" @default.
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