DNA polymerase can make mistakes while adding nucleotides. It edits the DNA by proofreading every newly added base. Incorrect bases are removed and replaced by the correct base, and then polymerization continues (Figure 6a). Most mistakes are corrected during replication, although when this does not happen, the mismatch repair mechanism is employed. Mismatch repair enzymes recognize the wrongly incorporated base and excise it from the DNA, replacing it with the correct base (Figure 6b). In yet another type of repair, nucleotide excision repair, the DNA double strand is unwound and separated, the incorrect bases are removed along with a few bases on the 5′ and 3′ end, and these are replaced by copying the template with the help of DNA polymerase (Figure 6c). Nucleotide excision repair is particularly important in correcting thymine dimers, which are primarily caused by ultraviolet light. In a thymine dimer, two thymine nucleotides adjacent to each other on one strand are covalently bonded to each other rather than their complementary bases. If the dimer is not removed and repaired it will lead to a mutation. Individuals with flaws in their nucleotide excision repair genes show extreme sensitivity to sunlight and develop skin cancers early in life.
DNA聚合酶在添加核苷酸时会出错。它通过校对每个新添加的碱基来编辑DNA。除去不正确的碱并用正确的碱代替，然后继续聚合（图6a）。大多数错误在复制过程中都会得到纠正，尽管这种情况不会发生，但会采用失配修复机制。错配修复酶识别错误掺入的碱基，并从DNA中切除碱基，并用正确的碱基替换（图6b）。在另一种修复方法中，即核苷酸切除修复，将DNA双链解开并分离，除去不正确的碱基以及5'和3'末端的一些碱基，并通过在帮助下复制模板来替换这些碱基DNA聚合酶的量（图6c）。核苷酸切除修复对于纠正主要由紫外线引起的胸腺嘧啶二聚体尤其重要。在胸腺嘧啶二聚体中，在一条链上彼此相邻的两个胸腺嘧啶核苷酸彼此共价键合，而不是它们的互补碱基。如果不去除和修复二聚体，将导致突变。核苷酸切除修复基因有缺陷的人表现出对日光的极度敏感性，并在生命早期发展为皮肤癌。