Abstract
While connexin46 (Cx46) and connexin50 (Cx50) are crucial for maintaining lens transparency and growth, the contributions of a more recently identified lens fiber connexin, Cx23, are poorly understood. Therefore, we studied the consequences of absence of Cx23 in mouse lenses. Cx23-null mice were generated by homologous Cre recombination. Cx23 mRNA was abundantly expressed in wild type lenses, but not in Cx23-null lenses. The transparency and refractive properties of Cx23-null lenses were similar to wild type lenses when examined by darkfield microscopy. Neither the focusing ability nor the light scattering was altered in the Cx23-null lenses. While both Cx46 and Cx50 localized to appositional fiber cell membranes (as in wild type lenses), their levels were consistently (but not significantly) decreased in homozygous Cx23-null lenses. These results suggest that although Cx23 expression can influence the abundance of the co-expressed lens fiber connexins, heterozygous or homozygous expression of a Cx23-null allele does not alter lens transparency.
Original language | English (US) |
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Pages (from-to) | 283-288 |
Number of pages | 6 |
Journal | Experimental eye research |
Volume | 146 |
DOIs | |
State | Published - May 1 2016 |
Funding
This work was supported by National Institutes of Health Grants RO1 EY08368 (ECB) and NS067550 (BP). The authors thank Linda Degenstein, technical director of the Transgenic Mouse and Embryonic Stem Cell Facility of the University of Chicago, who was instrumental in the generation of the Cx23-null mice.
Keywords
- Cataract
- Connexin
- Gap junction
- Knockout mouse
ASJC Scopus subject areas
- Ophthalmology
- Sensory Systems
- Cellular and Molecular Neuroscience