ERROR-PRONE DNA SYNTHESIS

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 病变旁路聚合酶可以合成与受损模板碱基相反的DNA，并被假设取代在病变部位停滞的复制性DNA聚合酶，从而允许DNA复制继续。存在这些聚合酶的几个亚家族，每个亚家族对一组独特的病变具有特异性。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。 我们希望在分子水平上了解这些聚合酶的病变特异性，复制过程中产生的错误类型，以及细胞中不同的DNA聚合酶是如何协调的，从而使复制准确而完整。

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.