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. 2022 Jun 29;607(7918):393–398. doi: 10.1038/s41586-022-04790-2

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© The Author(s) 2022

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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Extended Data Fig. 8 — (a) Structure of the DCL3–dsRNA complex (PDB: 7VG3). The amino-terminal helicase domain is disordered in the structure. (b) Model of the Dicer-2–dsRNA complex. The DCL3–dsRNA structure was superimposed onto the Dicer-2 structure, based on their RNase III domains, and DCL3 was then omitted. Predicted steric clashes are indicated by dashed circles. (c) Structure of the DCL1–dsRNA (pri-miRNA) complex (PDB: 7ELD). The carboxy-terminal RBDb domain is disordered in the structure. (d) Model of the Dicer-2–dsRNA complex. The Dicer-2 structure was predicted by AlphaFold2, and the dsRNA and CRBD were modeled based on the DCL3–dsRNA structure. Unstructured regions in the RIIIb and CL domains are omitted for clarity. In the model, the helicase domain interacts with the DUF283 domain and recognizes the dsRNA substrate, as in the DCL1–dsRNA structure.