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. 2023 Aug 24;14:5147. doi: 10.1038/s41467-023-40924-4

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© The Author(s) 2023

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — HUWE1 binds to WRNIP1 and both proteins prevent transcription-dependent TRCs. HUWE1 promotes the association of WRNIP1 with elongation-competent pS2-RNAPII. Upon induction of replication stress or in HUWE1-CS cells, WRNIP1 translocates from RNAPII to stalled replication forks, leading to stabilization of TRCs and recruitment of ATM to RNAPII via the MRN complex. Stabilization of the collision state induces ATM signaling and limits DNA breakage.