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. 2018 Sep 3;27(1):70–79. doi: 10.1038/s41431-018-0229-9

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© The Author(s) 2018

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. 3 — SPATC1L mRNA and protein levels in Hek293 transfected cells and Spatc1l expression in mouse whole cochlea and other tissues at different time points. a qRT-PCR analysis of relative mRNA expression of SPATC1L wild type and mutants after 48 h of transfection in Hek293 cells. Results are expressed as a fold-change of expression levels, and are normalized to the relative amount of the internal standard Neo. Error bars indicate 95% confidence intervals. b Western blot analysis of SPATC1L wild type and mutant proteins. Hsp90 was applied to determine equal loading. c The graph shows expression of Spatc1l in mouse whole cochlea at P3, P8, P12 and 2 months. Results are reported as fold change in gene expression over β actin, used as an internal control. The gene shows an age-related expression. d The graph shows Spatc1l expression at 2 months of age in different mouse tissues, including liver, cochlea, spleen, lung, kidney, brain, testis and heart. Results are reported as fold change in gene expression over β actin, used as an internal control