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. 2021 Feb 5;4:161. doi: 10.1038/s42003-021-01682-5

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© The Author(s) 2021

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. 6 — A, B Representative confocal microscopy images after immunocytochemical analyses showing similar localization of F-actin as visualized by phalloidin staining in control and CLN3 disease hiPSC-RPE cells (scale bar = 10 µm) (n = 3). Of note in panel B, orthogonal view of hiPSC-RPE monolayer shows expected apical localization of phalloidin relative to cell nuclei (DAPI) in control and CLN3 disease hiPSC-RPE. C–F Representative transmission electron microscopy (TEM) images (C, scale bar = 1 µm) and corresponding quantitative analyses showing decreased apical RPE microvilli density (D, p = 0.042), but similar apical-RPE microvilli width (E, p = 0.38), and length (F, p = 0.88) in control versus CLN3 disease hiPSC-RPE cells (n = 5). Two-tailed unpaired Student’s t-test performed for all statistical analysis. *p < 0.05.