As is often the case in most processes, things tend to become efficient as time passes. In a study focused on the effects of age on cell mutation day old and week old bacterial cells were used. When exposed to similar stimuli the older cells displayed a significantly higher level of mistranslation of proteins, with many of the surviving cells being unable to replicate. Although this result was not unexpected, the prevalent contributor to this enhanced level of mutation was determined to be the SOS repair response.
Odd… the SOS response is generally thought of as an absolute lifesaver for bacterial cells that have undergone extensive amounts of damage and most of the time it is. Cell pathology and death through mutation is commonly caused by the accumulation of multiple defects over time. When these defects accumulate to a high enough level that the usual methods of DNA repair are no longer sufficient to maintain cell function the SOS repair mechanism kicks in. Although this method is regulated by specific proteins, in this stage of repair where speed is more preferable to specificity for keeping the cell up and running, errors are more likely to occur. Coupled with the presence of previously accumulated errors the SOS response might just be adding fuel to the fire.
Primary Source:
Bacher, JM, Schimmel, P, (2006) An editing-defective aminoacyl-tRNA synthetase is
mutagenic in aging bacteria via the SOS response, PNAS, vol. 104, no. 2, pp.1907-1912
Secondary Sources:
Cirz, RT, et al. (2005) Inhibition of mutation and combating the evolution of antibiotic resistance, PLoS Biol 3(6): e176.
Nangle, LA, Motta, CM, Schimmel, P, (2006) Global Effects of Mistranslation from an Editing Defect in Mammalian Cells, Chemistry & Biology, vol 13, no. 10, pp. 1091-1100.
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