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 癌症和心脏病也有可能。 大多数诱变剂 在大多数生物体中， 修复（EPR）。 这种诱变剂的主要作用是破坏DNA， 阻止DNA复制复合体进展的方法。 EPR 然后在不良模板中促进损伤旁路（因此 诱变）方式。 uvsW是一个关键但神秘的基因， 噬菌体T4 EPR系统。 uvsW基因突变抑制了 重组，增加杀伤和消除诱变剂 通过EPR。 uvsW的温度敏感突变具有 通过映射和互补 试验及其对存活、重组和诱变的影响 已经确定。 uvsW的缺失突变已经被发现， 工程化，提供严格定义的无效等位基因。 的 uvsW的表达和调节正在由一个 DNA测序、Northern印迹、引物径流和 RNA测序方法。

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 mutations of uvsW has been engineered, providing a rigorously defined null allele. The expression and regulation of uvsW is being explored by a combination of DNA-sequencing, northern-blot, primer-runoff and RNA-sequencing methods.