Tunneling Nanotubes and the Eye: Intercellular Communication and Implications for Ocular Health and Disease

Figure 5

Phenotype of two Myo10 knockout mouse models. tm1d completely ablated all Myo10 forms, whereas tm2 selectively knocked out the full-length, actin-binding Myo10, but “headless” Myo10 expression was unaffected. (a) Fluorescence image of flat mounted retinas showing retinal vasculature at P5. Dissected retinas were stained with a PECAM-1 antibody (green) and counterstained with phalloidin (red). The retinal vasculature extended to similar positions in the control and Myo10^tm1d/tm1d eyes. The image represents a stitch of micrographs taken at 20x and is best visualized if the images are enlarged on a digital display. (b) High-resolution images of the angiogenic expansion front from the P5 retinas in (a) showing filopodia radiating from endothelial tips cells. Loss of Myo10 results in a decreased number of filopodia and leads to a less dense vascular network. Images were captured as Z-stacks at 60x and displayed as maximum projections with the PECAM-1 channel displayed in inverted grayscale to highlight endothelial filopodia. (c) High-resolution MRI (magnetic resonance imaging) of enucleated and fixed eyes from adult wild-type (WT) and Myo10^tm2/tm2 mice, where 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 toward the lens, as schematically illustrated on the right. Scale bars: 1 mm (reproduced from (a, b) Heimsath et al. 2017 and (c) Bachg et al. 2019 under the Creative Commons Attribution 4.0 International license (http://creativecommons.org/licenses/by/4.0/)) [105, 106].