REPLICATION REPAIR IN BACTERIOPHAGE T4

突变导致人类承受遗传出生的负担 缺陷和癌症，可能还有心脏病。 最 DNA损伤剂的致突变和致死作用是 是由DNA修复系统阻止的 经典描述的 系统在DNA复制之前修复损伤（通过直接 逆转或切除修复），在复制叉（通过 突变绕过受损的碱基）或复制后（通过 重组过程）。 我们最近发现了一种新的 在噬菌体T4中运作的修复模式。 资本主义则被定义为 几种突变增强了DNA损伤剂的杀伤作用。 这些突变存在于编码DNA酶的重要基因中 复制和修复出现日期，突变缺陷 在复制修复中，已经在编码 DNA解旋酶和SSB蛋白（其结合单链 DNA，将其保持在适合DNA的扩展配置中 复制）。 正在尝试寻找更多的突变 通过筛选编码T4的基因来影响这种修复过程 DNA引物酶和DNA聚合酶。

Mutagens contribute to the human burden of heritable birth defects and cancer and probably to heart disease as well. Most of the mutagenic and lethal effects of DNA-damaging agents are prevented by DNA repair systems. The classically described systems repair damage before DNA replication (by direct reversal or by excision repair), at the replication fork (by mutagenic bypass of damaged bases) or after replication (by a recombinational process). We have recently discovered a new mode of repair operating in bacteriophage T4. It is defined by several mutations that enhance killing by DNA-damaging agents. These mutations reside in vital genes encoding enzymes of DNA replication and repair appears to occur date, mutations defective in replication repair have been found in the genes encoding the DNA helicase and the SSB protein (which binds single-stranded DNA, holding it in an extended configuration suitable for DNA replication). Attempts are underway to find further mutations affecting this repair process by screening the genes encoding T4 DNA primase and DNA polymerase.