When replicative DNA polymerase encounters a thymine dimer, it cannot replicate past the site. Deoxyadenylate is 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 on the other side of 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.
Because the gap that is generated opposite a thymine dimer is created by faulty replication, the gap is close to the replication fork. Therefore, it is also close to the corresponding region on the other daughter duplex (Figure 25.15). If that region has itself not sustained damage, the RecA protein (E. coli) can initiate recombination between two homologous duplexes.
1. The uninvolved parental strand, which is complementary to the damaged parental strand, recombines into the gap, opposite the damaged site.
2. A gap now exists in the previously undamaged arm, but because it lies opposite an undamaged template, it can be filled by action of DNA polymerase and DNA ligase.
3. The thymine dimer itself is not repaired in this process, but the process allows time for the excision system to come in later and repair this damage.
RecA protein is required for daughter-strand gap repair, particularly in the first reaction, where the undamaged parental strand undergoes pairing with the parental strand opposite the gap.
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1. DNA Repair