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. 2023 Nov 25;14:7732. doi: 10.1038/s41467-023-43605-4

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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 — RBFOX2 (yellow) binds downstream of alternative exons to promote exon inclusion in key genes involved in insulin granule docking and exocytosis (including Stxbp1, Syt7, and Snap25). Splicing of these genes allows for proper docking and exocytosis of insulin granules. Loss of RBFOX2, results in mis-splicing of insulin granule docking and exocytosis genes. Causing a decrease in the docked pool of insulin granules and corresponding decrease in insulin secretion (created with BioRender.com).