ERROR-PRONE REPAIR IN 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）。 这些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（并且在那里 前诱变）方式。 因此，预期DNA聚合酶 在EPR中发挥着重要作用。 我们最近发现， 噬菌体T4 DNA聚合酶基因的突变可以增强 或抑制EPR。 最强的增强突变，hm（对于 超变的），也改变了EPR的特异性，优先 增加碱基对替换突变的频率。 虽然HM很难通过传统的杂交绘制地图， 现在已经将其归为DNA聚合酶基因。 我们还 确定了一些以前描述的DNA对EPR的影响 聚合酶突变，其中之一几乎废除EPR。 因此，在本发明中， T4 DNA聚合酶是数量的主要决定因素， EPR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.