Targeted Ablation of Connexin50 in Mice Results in Microphthalmia and Zonular Pulverulent Cataracts

摘要: In the ocular lens, gap junctional communication is a key component of homeostatic mechanisms preventing cataract formation. Gap junctions in rodent lens fibers contain two known intercellular channel-forming proteins, connexin50 (Cx50) and Cx46. Since targeted ablation Cx46 has been shown to cause senile-type nuclear opacities, it appears that Cx50 alone cannot meet requirements. To determine if pathology arises from reduction levels or loss connexin-specific function, we have generated mice with deletion gene. Cx50-null exhibited microphthalmia cataracts. At postnatal day 14 (P14), Cx50-knockout eyes weighed 32% less than controls, whereas mass was reduced by 46%. lenses also developed zonular pulverulent cataracts, abnormalities were detected P7. Deletion did not alter amounts distributions Cx43, epithelial junctions. addition, passage tracers revealed persistence between all cell types lens. These results demonstrate required only for maintenance transparency but normal eye growth. Furthermore, these data indicate unique functional properties both are proper development.