Biological repair mechanisms:  Low spontaneous mutation rates are evidence for the efficacy of biological repair mechanisms. See Table 10-4 for a summary of repair systems (in E. coli).  The principal mechanisms are error prevention, error reversal, excision repair, and post-replication repair. 

• Error prevention: The cellular machinery degrades damaging compounds, -e.g. superoxide dismutase and catylase degrade superoxide radicals.
• Error reversal: Enzymes reverse damage-causing events – e.g. phytolase can split the UV-induced photodimer which otherwise functions as a replication block and/or cause of nonspecific base insertion.  
• Excision repair: The general process involves removal of “incorrect” base(s) and replacement with the correct one(s).  This requires breaking the phosphodiester bonds on either side of the nucleotide(s) that will be replaced, replacement with the correct one(s) and resealing by ligase.
• Post-replication repair:  Mismatched bases (on the newly synthesized strand) are recognized after DNA replication.  Mismatched bases are excised and replaced: the template strand (source of the “correct code”) is distinguished from the newly synthesized strand by its methylation pattern.