ERROR-PRONE REPAIR IN 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)。这样的诱变剂，主要作用是破坏DNA在 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(并且 致突变前)的方式。因此，DNA聚合酶有望 在EPR中起着至关重要的作用。我们最近发现，某些 噬菌体T4 DNA聚合酶基因突变可增强 或抑制EPR。最强的增强突变，Hm(for 超变型)，也优先改变EPR的特异性 增加碱基对替换突变的频率。 尽管很难通过传统的杂交来定位hm，但我们 现已将其归类为DNA聚合酶基因。我们还有 确定了一些先前描述的DNA对EPR的影响 聚合酶突变，其中之一实际上废除了EPR。因此， T4DNA聚合酶是数量和 EPR的质量。

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 mutagans, 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 there fore mutagenic) manner. Thus, the DNA polymerase is expected to play a crucial role in EPR. We have recently found that certain mutations of the bacteriophage T4 DNA polymerase gene can enhance or suppress EPR. The strongest enhancing mutation, hm (for hypermutable), also changes the specificity of EPR, preferentially increasing the frequency of base pair substitution mutations. Although hm has been difficult to map by conventional crosses, we have now assigned it to the DNA polymerase gene. We have also ascertained the effect on EPR of some previously described DNA polymerase mutations, one of which virtually abolishes EPR. Thus, the T4 DNA polymerase is a major determinant of the quantity and quality of EPR.