ROLE OF GENE UVSW IN ERROR-PRONE REPAIR BY 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 大多数生物体中的诱变剂通过触发一种称为 易错修复（EPR） 这种诱变剂的主要作用是 以阻止DNA的进展的方式破坏DNA 复制复合体 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 噬菌体T4 EPR系统中关键但神秘的基因 并在一个不寻常的时间以少量表达， 噬菌体发育 uvsW的突变抑制了重组， 增加杀灭和消除诱变作用， EPR。 uvsW的温度敏感突变现在已经被 通过映射和互补产生和表征 试验及其对存活和诱变的影响正在 测定 已从质粒载体中分离到带有uvsW区域的质粒。 构建并将其缺失突变重新引入 T4染色体 这种突变将提供一个严格的 定义无效等位基因。 它和其他uvsW突变将用于 确定增加的羟基脲敏感性的基础 这是uvsW突变的诊断。 野生型uvsW基因 将置于质粒上， 基因产物的过度生产，其特性将 接受检查。

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 and is expressed in small amounts at an unusual time during phage development. Mutations in uvsW depress recombination, increase killing and abolish mutagenesis by agents acting through EPR. Temperature-sensitive mutations of uvsW have now been generated and characterized by mapping and complimentation tests and their effects on survival and mutagenesis are being determined. A plasmid bearing and uvsW region has been constructed and a deletion mutation thereof reintroduced into the T4 chromosome. This mutation will provide a rigorously defined null allele. It and other uvsW mutations will be used to determine the basis of the increased hydroxyurea sensitivity which is diagnostic of uvsW mutations. The wild-type uvsW gene will be placed on a plasmid under conditions suitable for overproduction of the gene product, whose properties will then be examined.