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. 2020 Apr 17;11(4):240. doi: 10.1038/s41419-020-2443-y

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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. 7 — Schematic representation of the combinatorial control of Spo11 alternative splicing elicited by RNAPII dynamics and hnRNPH or Sam68 recruitment. At P14, the fast elongation rate of RNAPII promotes recruitment of Sam68 and inclusion of exon 2, thus yielding SPO11β. At P18, reduction of the speed of RNAPII favors recruitment of hnRNPH, which competes out Sam68 and promotes exon 2 skipping and SPO11α splicing.