Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA.
Genes Dev. 2021 Oct 1;35(19-20):1339-1355. doi: 10.1101/gad.348517.121. Epub 2021 Sep 23.
Prior to initiation of DNA replication, the eukaryotic helicase, Mcm2-7, must be activated to unwind DNA at replication start sites in early S phase. To study helicase activation within origin chromatin, we constructed a conditional mutant of the polymerase α subunit Cdc17 (or Pol1) to prevent priming and block replication. Recovery of these cells at permissive conditions resulted in the generation of unreplicated gaps at origins, likely due to helicase activation prior to replication initiation. We used micrococcal nuclease (MNase)-based chromatin occupancy profiling under restrictive conditions to study chromatin dynamics associated with helicase activation. Helicase activation in the absence of DNA replication resulted in the disruption and disorganization of chromatin, which extends up to 1 kb from early, efficient replication origins. The CMG holohelicase complex also moves the same distance out from the origin, producing single-stranded DNA that activates the intra-S-phase checkpoint. Loss of the checkpoint did not regulate the progression and stalling of the CMG complex but rather resulted in the disruption of chromatin at both early and late origins. Finally, we found that the local sequence context regulates helicase progression in the absence of DNA replication, suggesting that the helicase is intrinsically less processive when uncoupled from replication.
在启动 DNA 复制之前,真核解旋酶 Mcm2-7 必须被激活,以在早期 S 期的复制起始位点解开 DNA。为了在起始点染色质中研究解旋酶的激活,我们构建了聚合酶α亚基 Cdc17(或 Pol1)的条件性突变体,以阻止引发并阻断复制。在允许的条件下恢复这些细胞,会在起始点产生未复制的缺口,这可能是由于复制起始前解旋酶的激活。我们在限制条件下使用微球菌核酸酶(MNase)为基础的染色质占有率分析来研究与解旋酶激活相关的染色质动力学。在没有 DNA 复制的情况下,解旋酶的激活导致染色质的破坏和紊乱,这种情况从早期、有效的复制起始点延伸了 1 kb 以上。CMG 全酶复合物也从起始点移动相同的距离,产生单链 DNA,激活细胞内 S 期检查点。检查点的缺失不会调节 CMG 复合物的进展和停滞,而是导致早期和晚期起始点的染色质破坏。最后,我们发现,在没有 DNA 复制的情况下,局部序列环境调节解旋酶的进展,这表明解旋酶在与复制解耦时内在地缺乏连续性。