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Publication : Ectopic Rod Photoreceptor Development in Mice with Genetic Deficiency of WNT2B.

First Author  Blomfield AK Year  2023
Journal  Cells Volume  12
Issue  7 PubMed ID  37048106
Mgi Jnum  J:334742 Mgi Id  MGI:7462771
Doi  10.3390/cells12071033 Citation  Blomfield AK, et al. (2023) Ectopic Rod Photoreceptor Development in Mice with Genetic Deficiency of WNT2B. Cells 12(7)
abstractText  Wnt/beta-catenin signaling is essential for embryonic eye development in both the anterior eye and retina. WNT2B, a ligand and activator of the Wnt/beta-catenin pathway, assists in the development of the lens and peripheral regions of the eye. In humans WNT2B mutations are associated with coloboma and WNT2B may also assist in retinal progenitor cell differentiation in chicken, yet the potential role of WNT2B in retinal neuronal development is understudied. This study explored the effects of WNT2B on retinal neuronal and vascular formation using systemic Wnt2b knockout (KO) mice generated by crossing Wnt2b(flox/flox) (fl/fl) mice with CMV-cre mice. Wnt2b KO eyes exhibited relatively normal anterior segments and retinal vasculature. Ectopic formation of rod photoreceptor cells in the subretinal space was observed in Wnt2b KO mice as early as one week postnatally and persisted through nine-month-old mice. Other retinal neuronal layers showed normal organization in both thickness and lamination, without detectable signs of retinal thinning. The presence of abnormal photoreceptor genesis was also observed in heterozygous Wnt2b mice, and occasionally in wild type mice with decreased Wnt2b expression levels. Expression of Wnt2b was found to be enriched in the retinal pigment epithelium compared with whole retina. Together these findings suggest that WNT2B is potentially involved in rod photoreceptor genesis during eye development; however, potential influence by a yet unknown genetic factor is also possible.
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