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In bacteria, high mutation rate associated to mutator genes allow rapid adaptation to new selective conditions [58].
This can be attributed, in part, to the high mutation rate associated with RNA viral replication, which favors the emergence of drug resistance and limits the efficacy of current therapies.
The reasons behind this are unclear, especially given the high mutation rate associated with influenza virus replication.
Genetic diversity in influenza virus results from a high mutation rate associated with replication using a low-fidelity RNA polymerase and the reshuffling (reassortment) of segments among coinfecting strains.
Instead, they implicate a higher mutation rate associated with the presence of the indel.
The most plausible explanation will be to allow for the increase in the mutation rate associated with the ageing of stem cells.
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Current evidence of the molecular events affecting quasispecies dynamics suggests that it is unlikely that a viral population can acquire mutational robustness under the increased mutation rates associated with mutagenic treatments.
If the mutation rates associated with stem cells are a lot higher than the mutation rates of daughter cells, then few stem cells per crypt is the evolutionarily optimal strategy.
In most cases, higher numbers of stem cells per crypt correspond to lowering the chance of colon cancer initiation (except if mutation rates associated with daughter cells are a lot lower than those associated with stem cells).
The accelerated mutation rates associated with the cyclic peptide domains could reflect either a strong positive selection or specific hypermutation.
Is higher accuracy (lower mutation rates) associated with slower copying of DNA (and therefore more time for checking of potential errors during copying)?
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CEO of Professional Science Editing for Scientists @ prosciediting.com