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. 2017 Oct 31;8:1220. doi: 10.1038/s41467-017-01332-7

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© The Author(s) 2017

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 — Transgenic removal of RBCs from developing circuits. a Section through a Grm6L-YFP-DTA ^con retina in which ON bipolar cells express YFP (green) stained for VGluT1 (blue), which labels photoreceptor and bipolar cell axon terminals, and for the RBC-specific marker PKCα (red). Scale bar indicates 20 μm. b–d Retinal flat mounts from wild-type (b), Pcp2-DTA (c), and Pax6-DTA (d) mice stained for PKCα. Scale bar indicates 20 μm. e Summary data (mean ± SEM) of RBC densities in wild-type (n = 23 mice), Pcp2-DTA (n = 8 mice), and Pax6-DTA (n = 22 mice) mice. By Kruskal–Wallis one-way ANOVA testing, the density of RBCs was lower in Pcp2-DTA and Pax6-DTA compared to wild-type retinas (p < 0.04 and p < 10⁻⁸, respectively), and lower in Pax6-DTA than in Pcp2-DTA retinas (p < 0.049)