Postreplication repair refers to processes that attempt to fix mismatches, gaps, or damage to DNA that escape the repair processes that occur during replication (such as proofreading--see here).

When a replicative polymerase encounters a thymine dimer, it cannot replicate past the site. Deoxyadenylate can be incorporated opposite the first thymine base in the template, but the double helix distortion induced by the thymine dimer, causes the structure to be recognized as a mismatch, and the polymerase "idles" at the damage site, converting dATP to dAMP by a continual process of insertion and exonucleolytic cleavage (due to proofreading).

Synthesis of an Okazaki fragment (see here) can commence opposite the damaged site, leaving a gap opposite the thymine dimer. The gap would be lethal if unrepaired, however, because it would generate a double-strand break in the next round of replication.

Two distinct processes can repair the gap:

1. Recombinational repair, or daughter-strand gap repair

2. SOS response, or error-prone repair

Both processes depend critically (in E. coli) on a protein called RecA.

Another postreplication repair system is that of mismatch repair, which can repair replication mistakes that escape proofreading or which arise from chemical alteration of bases, such as deamination of cytosine to form uracil.