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. 2018 Jul 9;8:10360. doi: 10.1038/s41598-018-28511-w

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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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il10^e46 point mutation in the exon 1 of the il10 results in a premature stop codon but does not alter il10 expression. (a) A schematic presentation of the il10^e46 mutation; a adenosine (A) to thymidine (T) point mutation results in a stop codon (TAA) after the first 27 amino acids in exon 1. (b) Relative il10 expression was measured with qPCR in unchallenged il10^e46/e46 mutant and WT zebrafish, spleen and liver from the same individuals (n = 10 in both groups) and is presented as a scatter dot blot and median. Note the divided y axis. Gene expressions were normalized to the expression of eef1a1l1. A two-tailed Mann-Whitney test was used for the statistical comparison of differences between il10^e46/e46 zebrafish and WT controls.