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. 2020 Dec 18;52(12):1948–1958. doi: 10.1038/s12276-020-00533-3

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — a During normal replication, ATAD5-RLC and ATAD5/UAF1-interacting DNA/RNA helicases migrate with a replication fork. ATAD5/UAF1-interacting DNA/RNA helicases resolve R-loops ahead of the replication fork and facilitate replication fork progression. Upon replication stress, which increases transcription–replication conflicts and unscheduled R-loop formation, additional DNA/RNA helicases are recruited to the replication fork, which resolves R-loops to ensure faithful replication fork progression. Under both normal and replication stress conditions, the recruitment of helicases at the replication fork is dependent on the ATAD5/UAF1 interaction. b In ATAD5-depleted cells, reduced R-loop resolution by ATAD5/UAF1-interacting DNA/RNA helicases leads to defects in replication fork progression. In addition, PCNA and its interacting proteins accumulated on lagging strand DNA behind the forks collide with transcription machinery, which consequently increases R-loop formation at the collision site.