Sloppier copier DNA polymerases involved in genome repair
Sloppier copier DNA polymerases involved in genome repair
复制标题
DOI：
10.1016/s0959-437x(00)00057-5
复制
发表时间：
2000-04-01
影响因子：
4
通讯作者：
Tippin, B
中科院分区：
文献类型：
--
作者：
Goodman, MF;Tippin, B
当染色体复制在DNA损伤的存在下受阻时，新发现的原核和真核DNA聚合酶的UmuC/DinB/Rev 1/Rad 30超家族的成员在被阻断的复制叉处催化translesion合成。虽然这些聚合酶共享基本上与标准复制和修复酶无关的序列元件，但它们中的一些（如SOS诱导的大肠杆菌pol V）催化“易错”的translesion合成，导致突变的大幅增加，而其他的（一个例子是着色性干皮病变体基因产物XPV pol eta）进行异常但非致突变的translesion合成。对这些低保真度聚合酶的持续研究可以为体细胞超突变机制提供新的见解，体细胞超突变是免疫反应中的关键因素。
When chromosomal replication is impeded in the presence of DNA damage, members of a newly discovered UmuC/DinB/Rev1/Rad30 superfamily of procaryotic and eucaryotic DNA polymerases catalyze translesion synthesis at blocked replication forks. Although these polymerases share sequence elements essentially unrelated to the standard replication and repair enzymes, some of them (such as the SOS-induced Escherichia coli pol V) catalyze 'error-prone' translesion synthesis leading to large increases in mutation, whereas others (an example being the Xeroderma pigmentosum variant gene product XPV pol eta) carry out aberrant, yet nonmutagenic translesion synthesis. Ongoing studies of these low fidelity polymerases could provide new insights into the mechanism of somatic hypermutation, a key element in the immune response.