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. 2019 Jan 24;9:597. doi: 10.1038/s41598-018-37160-y

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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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High penetrance of persistence of the hyaloid vasculature, without retinal hypovascularization, in Myo10^tm2/tm2 mice. (A) High-resolution MRI (magnetic resonance imaging) of enucleated and fixed eyes from adult wild-type (WT) and Myo10^tm2/tm2 mice (representative of 6 eye scans for each genotype) reveals persistence of the hyaloid vasculature in mutant mice. The hyaloid artery emerges from the optic disc and extends towards the lens, as schematically illustrated on the right. Scale bars: 1 mm. (B) Whole-mount retina from an adult WT and Myo10^tm2/tm2 mouse stained with anti-collagen, type IV antibodies. Hyaloid vessels can be seen emerging from the central optic disc of the Myo10^tm2/tm2 retina. Scale bar: 1 mm. (C) Schematic diagram showing putative roles of Myo10 in macrophage-to-endothelial cell Wnt signaling, and knockout mouse models in which hyaloid persistence phenotypes, with or without retinal hypovascularization, manifest. Notably, Wnt7b^d1 is a hypomorphic allele, implying that there is reduced, but not absent, Wnt7b gene function in Wnt7b^d1/d1 mice. PU.1 null (PU.1−/−) mice lack macrophages.