ERROR-PRONE DNA SYNTHESIS

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 病变旁路聚合酶可以合成与受损模板碱基相反的DNA，并被假设为取代在病变部位停滞不前的复制型DNA聚合酶，使DNA复制继续进行。存在这些聚合酶的几个亚家族，每个亚家族都表现出对一组独特的病变的特异性。当复制未受损的DNA时，病变旁路聚合酶具有非常高的错误率。我们想要在分子水平上了解这些聚合酶的损伤特异性，复制过程中出错的类型，以及细胞中不同的DNA聚合酶是如何协调的，从而使复制准确和完整。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The lesion-bypass polymerases can synthesize DNA opposite damaged template bases and are hypothesized to replace replicative DNA polymerases that stall at lesion sites, allowing DNA replication to continue. Several subfamilies of these polymerases exist, with each displaying specificity for a unique set of lesions. When replicating undamaged DNA, the lesion-bypass polymerases have a very high error rate. We want to understand, at the molecular level, the lesion specificity of these polymerases, the types of errors made during replication, and how the different DNA polymerases in a cell are all coordinated so that replication is accurate and complete.