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. 2020 Oct 27;10:17894. doi: 10.1038/s41598-020-74800-8

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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 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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Rbm20^S637A/S637A and Rbm20^KO/KO mice are defective in RBM20-dependent alternative splicing. (a) RT-PCR analysis of Ttn mRNAs with exon (E) 50 forward, E51 reverse and E219 reverse primers (top), E50 forward, E215 forward and E219 reverse primers (middle) and E115 forward, E215 forward and E219 reverse primers (bottom). Splicing patterns of the PCR products and names of corresponding titin isoforms are indicated on the right. (b) RT-PCR analysis of Ldb3 (top), Camk2d (middle), and Ryr2 (bottom) mRNAs. Gel-like images by Bioanalyzer (Agilent) are shown (a,b). (c) Vertical SDS-agarose gel electrophoresis and CBB staining of cardiac proteins from the hearts of 4-week-old Rbm20 mutant mice. Genotypes of the individual mice are indicated above. Titin isoforms (N2B, N2BA and N2BA-G) and myosin heavy chain (MHC) are indicated. n = 3 mice (a–c), each showing similar results. Full length original images are shown in Supplementary Information.