The reprogramming process itself can contribute to mutation rates: nuclear genomic mutations arise during reprogramming and are selected against during subsequent culture (Hussein et al., 2011).
Although there are limited data so far, there is an expectation that mobile element insertions will contribute to mutation of driver genes in cancers.
At the same time, our postulated saturation-induced mutator phenotype might contribute to mutations in genes encoding proteins that act in DNA repair, such as mutS, resulting in hypermutable P. aeruginosa strains.
Diesel exhaust and many individual substances contained in it (including arsenic, benzene, formaldehyde and nickel) have the potential to contribute to mutations in cells that can lead to cancer.
There are multiple factors that could contribute to mutations.
Consistent with this hypothesis, DinB contributes to mutations in mucA that promote alginate production under laboratory conditions [34].
Finally, since error-prone repair or TLS of oxidized DNA lesions will contribute to mutations, we hypothesized that MutS and DinB play opposing roles in P. aeruginosa pathoadaptation.
This reduced fidelity is vital to their ability to catalyze TLS, and, together with the miscoding or non-coding nature of many lesions, explains why TLS can be error-prone, contributing to mutations.
Taken together, these results suggest that DinB contributes to mutations by catalyzing error-prone bypass of one or more oxidized DNA lesions other than 8-oxo-dG in vivo.
