REPLICATION REPAIR IN BACTERIOPHAGE T4

诱变剂增加了人类可遗传生育的负担 缺陷和癌症，可能还有心脏病。多数 DNA损伤剂的诱变和致死作用有 通过DNA修复系统进行预防。经典的描述 系统在DNA复制之前修复损坏(通过直接 反转或通过切除修复)，在复制分叉(通过 破坏碱基的突变旁路)或在复制之后(通过 重组过程)。我们最近发现了一种新的 T4噬菌体的修复模式。它由以下定义 几种突变可以增强DNA损伤剂的杀伤力。 这些突变存在于编码dna酶的重要基因中。 复制和修复似乎发生在日期，突变有缺陷 在编码复制修复的基因中发现了 DNA解旋酶和SSB蛋白(与单链结合 DNA，将其保持在适合DNA的扩展配置中 复制)。目前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启动酶和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.