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. 2020 Oct 27;10:18378. doi: 10.1038/s41598-020-75375-0

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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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A phosphomimetic S315D mutation in mmCx36 did not change the size of mmCx36-containing gap junctions. HEK293 cells transfected either with mmCx36 WT (a), the S315D mutant (b), which mimics the phosphorylation of S315 in mmCx36, or a truncated Cx36 variant (c). Gap junctions were detected between adjacent cells and reconstructed (d). (e) Quantification of gap junction volume showed that the S315D mutation did not alter gap junction size in transfected HEK293 cells, in contrast to the truncation which led to significantly smaller gap junctions. Values are given as mean ± SD; n.s., not significant; **p < 0.01; Mann–Whitney test, n = 123/138 cell pairs from 4 transfections. Scale: 10 µm.