Cox Michael M
Department of Biochemistry, University of Wisconsin at Madison, 433 Babcock Drive, Madison, WI 53706-1544, USA.
Mutat Res. 2002 Dec 29;510(1-2):107-20. doi: 10.1016/s0027-5107(02)00256-7.
When replication forks stall or collapse at sites of DNA damage, there are two avenues for fork rescue. Mutagenic translesion synthesis by a special class of DNA polymerases can move a fork past the damage, but can leave behind mutations. The alternative nonmutagenic pathways for fork repair involve cellular recombination systems. In bacteria, nonmutagenic repair of replication forks may occur as often as once per cell per generation, and is the favored path for fork restoration under normal growth conditions. Replication fork repair is almost certainly the major function of bacterial recombination systems, and was probably the impetus for the evolution of recombination systems. Increasingly, the nonmutagenic repair of replication forks is seen as a major function of eukaryotic recombination systems as well.
当复制叉在DNA损伤位点停滞或崩溃时,有两条途径可以拯救复制叉。一类特殊的DNA聚合酶进行的易错跨损伤合成可以使复制叉越过损伤部位,但会留下突变。复制叉修复的另一种无突变途径涉及细胞重组系统。在细菌中,复制叉的无突变修复可能每代每个细胞发生一次,并且是正常生长条件下复制叉恢复的首选途径。复制叉修复几乎肯定是细菌重组系统的主要功能,并且可能是重组系统进化的推动力。越来越多的证据表明,复制叉的无突变修复也是真核生物重组系统的主要功能。