Podust V N, Hübscher U
Department of Veterinary Biochemistry, University Zürich-Irchel, Switzerland.
Nucleic Acids Res. 1993 Feb 25;21(4):841-6. doi: 10.1093/nar/21.4.841.
By using a defined gapped DNA substrate that mimics a lagging strand of 230 nucleotides and that contains a defined pause site, we have analyzed calf thymus DNA polymerases (pol) alpha, beta, delta, and epsilon in the presence of the three auxiliary proteins proliferating cell nuclear antigen (PCNA), replication factor C (RF-C) and replication protein A (RP-A) for their ability to complete an Okazaki fragment. Pol alpha alone could fill the gap to near completion, but was strongly stopped by the pause site. Addition of low amounts of RP-A resulted in an increased synthesis by pol alpha past the pause site. In contrast, high amounts of RP-A strongly inhibited gap filling by pol alpha. Further inhibition was evident when the two other auxiliary proteins, PCNA and RF-C, were added in addition to RP-A. Pol beta could completely fill the gap without specific pausing and also was strongly inhibited by RP-A. PCNA and RF-C had no detectable effect on pol beta. Pol delta, relied as expected, on all three auxiliary proteins for complete gap filling synthesis and could, upon longer incubation, perform a limited amount of strand displacement synthesis. Pol epsilon core enzyme was able to fill the gap completely, but like pol alpha, essentially stopped at the pause site. This pausing could only be overcome upon addition of PCNA, RF-C and E. coli single-stranded DNA binding protein. Thus pol epsilon holoenzyme preferentially synthesized to the end of the gap without pausing. Ligation of the DNA products indicated that pol beta core enzyme, pol delta and pol epsilon holoenzymes (but not pol alpha and pol epsilon core enzyme) synthesized products that were easily ligatable. Our results indicate that pol epsilon holoenzyme fills a defined lagging strand gapped template to exact completion and is able to pass a pause site. The data favour the hypothesis of Burgers (Burgers, P.M.J. (1991) J. Biol. Chem. 266, 22698-22706) that pol epsilon might be a candidate for the second replication enzyme at the lagging strand of the replication fork.
通过使用一种特定的带缺口的DNA底物,该底物模拟一条230个核苷酸的滞后链并含有一个特定的暂停位点,我们分析了小牛胸腺DNA聚合酶(pol)α、β、δ和ε在三种辅助蛋白增殖细胞核抗原(PCNA)、复制因子C(RF-C)和复制蛋白A(RP-A)存在的情况下完成冈崎片段的能力。单独的polα能够将缺口填充至接近完成,但被暂停位点强烈阻止。添加少量的RP-A会导致polα在暂停位点之后的合成增加。相反,大量的RP-A会强烈抑制polα的缺口填充。当除了RP-A之外还添加另外两种辅助蛋白PCNA和RF-C时,进一步的抑制作用很明显。polβ能够完全填充缺口而没有特定的暂停,并且也被RP-A强烈抑制。PCNA和RF-C对polβ没有可检测到的影响。正如预期的那样,polδ依赖于所有三种辅助蛋白来完成完整的缺口填充合成,并且在较长时间孵育后能够进行有限量的链置换合成。polε核心酶能够完全填充缺口,但与polα一样,基本上在暂停位点处停止。只有在添加PCNA、RF-C和大肠杆菌单链DNA结合蛋白后才能克服这种暂停。因此,polε全酶优先合成至缺口末端而不暂停。DNA产物的连接表明,polβ核心酶、polδ和polε全酶(但不是polα和polε核心酶)合成的产物易于连接。我们的结果表明,polε全酶能够将特定的滞后链带缺口模板精确填充至完成,并能够通过一个暂停位点。这些数据支持了Burgers的假设(Burgers, P.M.J. (1991) J. Biol. Chem. 266, 22698 - 22706),即polε可能是复制叉滞后链上第二种复制酶的候选者。