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. 2019 Nov 13;9:16669. doi: 10.1038/s41598-019-52848-5

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© The Author(s) 2019

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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Lack of N-terminal actin acetylation in HAP1 cells leads to a dramatic increase in N-terminal β-actin arginylation level. Left, Western blots of HAP1 WT, HAP1 NAA80 knockout and 100% confluent MEF cells. Middle, quantification and comparison of the R-actin fluorescence signal from these different cell types. Signal of total protein stain was used as reference for R-actin normalization. The 5.3% arginylation in HAP1NAA80KO cells is shown as an estimate, since no β-actin signal can be detected in these cells. Right, quantification of the percentage of R-actin in wild type HAP1. Error bars represent SEM, n = 5, Student’s t-test was used to determine the P value.