ROLE OF GENE UVSX 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。噬菌体T4 uvsX基因在EPR和重组中起着重要作用。其 产物是重组酶，一种催化同源链 DNA分子之间的交换。该蛋白在EPR中的特殊作用 依然神秘。尽管uvsX的几个严重突变仅 半致命，有迹象表明，一个更剧烈的破坏uvsX 可能是致命的因此，突变被引入早期 检测基因的部分和产生的突变体的表型， 包括生存能力。这些突变体与 典型的uvsX突变体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. The bacteriophage T4 uvsX gene plays a central role in EPR and also in recombination. Its product is a recombinase, a protein that catalyzes homologous strand exchange between DNA molecules. The specific role of this protein in EPR remains mysterious. Although several severe mutations of uvsX are only semilethal, there are hints that an even more drastic disruption of uvsX might be fully lethal. Therefore, mutations were introduced into early parts of the gene and the resulting mutants were examined for phenotype, including viability. These mutants were not substantially different from the canonical uvsX mutant. This work is now in press and the project is completed.