ROLE OF GENE UVSW IN ERROR-PRONE REPAIR BY BACTERIOPHAGE T4

突变导致人类遗传性出生缺陷的负担， 癌症，可能也会导致心脏病。大多数诱变剂 生物体通过触发一种称为易错修复（EPR）的过程来发挥作用。等 诱变剂的主要作用是破坏DNA，从而阻止基因突变的进程。 DNA复制复合体的一部分EPR然后促进损伤旁路， 不好的模板（因此是诱变的）方式。uvsW是一个关键， 噬菌体T4 EPR系统中的神秘基因。uvsW突变 抑制重组、增加杀伤和消除试剂的诱变 通过EPR。uvsW的温度敏感性突变已经被 通过映射和互补测试生成和表征， 已经确定了对存活、重组和诱变的影响。一 已经设计了uvsW的缺失突变，提供了严格的 定义无效等位基因。这项工作现在正在印刷中，该项目是 完成

Mutagens contribute to the human burden of heritable birth defects and cancer and probably to heart disease as well. Most mutagens in most organisms act by triggering a process called error-prone repair (EPR). Such mutagens' primary action is to damage DNA in ways that block the progress of the DNA replication complex. EPR then facilitates damage bypass in a poorly templated (and therefore mutagenic) manner. uvsW is a crucial but mysterious gene in the bacteriophage T4 EPR system. Mutations in uvsW depress recombination, increase killing and abolish mutagenesis by agents acting through EPR. Temperature-sensitive mutations of uvsW have been generated and characterized by mapping and complementation tests and their effects on survival, recombination and mutagenesis have been determined. A deletion mutation of uvsW has been engineered, providing a rigorously defined null allele. This work is now in press and the project is completed.