Madison B Adolph, Garrett M Warren, Frank B Couch, Briana H Greer, Brandt F Eichman, David Cortez
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引用次数: 0
摘要
在 DNA 复制过程中，复制体会遇到各种障碍，包括 DNA 损伤、转录-复制冲突以及其他复制压力源。必须有效克服这些障碍，才能完成 DNA 合成，并将基因组的不稳定性降至最低。耐受复制压力的途径之一是复制叉逆转，在这一过程中，亲代模板 DNA 链重新接合，并形成新生-新生 DNA 双链。有几种酶能促进复制叉逆转，包括依赖 ATP 的转位酶 SMARCAL1、ZRANB3 和 HLTF。这些酶如何在含有分叉分离病变的 DNA 上进行转位尚不清楚。在这里，我们研究了 SMARCAL1、ZRANB3 和 HLTF 对前导或滞后模板链上各种病变的耐受能力。我们证明，SMARCAL1 和 ZRANB3 会选择性地抑制前导模板链上的病变，而 HLTF 对任一模板链上的大块病变都不敏感。这些结果表明，在分叉逆转过程中，SMARCAL1 和 ZRANB3 与前导链接触，因此对该链上大块病变的抑制更敏感。相比之下，HLTF DNA 易位对 DNA 损伤不敏感。叉形反转酶之间的这些生化差异使人们对它们的DNA重塑机制有了更深入的了解，并表明它们可能在特异性病变环境中发挥作用。
WITHDRAWN: Strand dependent bypass of DNA lesions during fork reversal by ATP-dependent translocases SMARCAL1, ZRANB3, and HLTF.
The authors have withdrawn this manuscript because they identified problems with how some figure panels were processed. Those experiments will be repeated before deposition of a new manuscript. Therefore, the authors do not wish this work to be cited as reference for the project. If you have any questions, please contact the corresponding authors.
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