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

诱变剂增加了人类可遗传出生缺陷的负担 以及癌症，可能还会导致心脏病。大多数诱变剂 在大多数生物中，行为是通过触发一个称为容易出错的过程来实现的 修复(EPR)。这种诱变剂的主要作用是破坏DNA 阻碍DNA复制复合体进展的方法。EPR 然后便于在糟糕的模板中绕过损害(因此 致突变的)方式。Uvsw是一种关键但神秘的基因 噬菌体T4 EPR系统。UvsW基因突变抑制 重组、增加杀伤力和取消毒剂的诱变 通过EPR采取行动。UvsW的温度敏感突变有 通过映射和互补来生成和表征 试验及其对生存、重组和诱变的影响 已经确定了。UvsW的一种缺失突变已被 设计的，提供严格定义的零等位基因。这个 Uvsw的表达和调控正在由一个 DNA测序、Northern-Blot、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.