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. 2018 May;1864(5Part A):1609–1621. doi: 10.1016/j.bbadis.2018.01.028

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© 2018 The Authors

This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

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Fig. 3 — Vps33b and Vipar deficient skin disease is not caused by defects in epidermal junctions. A - Claudin-1 and E-cadherin staining in control, Vps33b^fl/flER^T2 and Vipas39^fl/flER^T2 skin sections, counterstained with DAPI. Scale bars = 20 μm. Dermo-epidermal junction (dashed line). B - β-catenin staining in control, Vps33b^fl/flER^T2 and Vipas39^fl/flER^T2 skin sections counterstained with DAPI. Scale bars = 20 μm. Immunofluorescent images are single z-slices from a z-stack and are representative of results from at least six control and three Vps33b^fl/flER^T2 and Vipas39^fl/flER^T2 independent murine biopsies. C - TEER readings of control and Vps33b^fl/flER^T2 keratinocyte cultures. Results from two experiments are shown with different symbols. D - TEER readings of individual control Vipas39^fl/flER^T2 keratinocyte cultures. E - TEM images of desmosomes between adjacent keratinocytes in control, Vps33b^fl/flER^T2 and Vipas39^fl/flER^T2 epidermis. Scale bars = 400 nm. TEM images are representative of at least two independent murine biopsies per genotype.