Abstract
The role of the core planar cell polarity (PCP) pathway protein, Vangl2, was investigated in the corneal epithelium of the mammalian eye, a paradigm anatomical model of planar cell migration. The gene was conditionally knocked out in vivo and knocked down by siRNA, followed by immunohistochemical, behavioural and morphological analysis of corneal epithelial cells. The primary defects observed in vivo were of apical-basal organisation of the corneal epithelium, with abnormal stratification throughout life, mislocalisation of the cell membrane protein, Scribble, to the basal side of cells, and partial loss of the epithelial basement membrane. Planar defects in migration after wounding and in presence of an applied electric field were noted. However, knockdown of Vangl2 also retarded cell migration in individual cells that had no contact with their neighbours, which precluded a classic PCP mechanism. It is concluded that some of the planar polarity phenotypes in PCP mutants may arise from disruption of apical-basal polarity.
Original language | English |
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Pages (from-to) | 106-119 |
Number of pages | 14 |
Journal | Journal of Anatomy |
Volume | 234 |
Issue number | 1 |
Early online date | 17 Aug 2017 |
DOIs | |
Publication status | Published - Jan 2019 |
Bibliographical note
This work was performed under Biotechnology and Biological Sciences Research Council (BBSRC) research grant BB/J015237/1 to JMC. DAP was funded by an Anatomical Society PhD Studentship whose support is gratefully acknowledged. ASF was funded by a BBSRC DTG PhD Studentship. We thank staff at the Medical Research Facility and Aberdeen Microscopy Services for technical assistance.Keywords
- cornea
- epithelium
- planar cell polarity
- Vangl2
- apical-basal polarity