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. 2023 May 10;617(7962):842–850. doi: 10.1038/s41586-023-06049-w

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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. 4 — a, Interactions between the subunits of the molecular brake. Interacting residues are shown as spheres depicted in the same colour as their binding partner. The domains of PRP2 RecA1, RecA2, HB and NTD are depicted. The anchoring surfaces of the brake elements to PRP8 (grey oval) are indicated. The inset shows a schematic representation of the molecular brake, in which the subunits are coloured as in the surface and cartoon representation. CWC15 is yellow. b, Interactions of the intron with PRP2^NTD, PPIL4 and SKIP. c, Interactions of PPIL4 with CWC15 and SKIP. d,e, The wedge element of SKIP intercalates between RecA1, RecA2 and the HB domains of PRP2, indicating inhibition of translocation. PPIL4, SKIP and CWC15 are red, cyan and yellow, respectively.