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 of Cx46 has been shown to cause senile-type nuclear opacities, it appears that Cx50 alone cannot meet homeostatic requirements. To determine if lens pathology arises from a reduction in levels of communication or the loss of a connexin-specific function, we have generated mice with a targeted deletion of the Cx50 gene. Cx50-null mice exhibited microphthalmia and nuclear cataracts. At postnatal day 14 (P14), Cx50-knockout eyes weighed 32% less than controls, whereas lens mass was reduced by 46%. Cx50-knockout lenses also developed zonular pulverulent cataracts, and lens abnormalities were detected by P7. Deletion of Cx50 did not alter the amounts or distributions of Cx46 or Cx43, a component of lens epithelial junctions. In addition, intercellular passage of tracers revealed the persistence of communication between all cell types in the Cx50-knockout lens. These results demonstrate that Cx50 is required not only for maintenance of lens transparency but also for normal eye growth. Furthermore, these data indicate that unique functional properties of both Cx46 and Cx50 are required for proper lens development.
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2 November 1998
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November 02 1998
Targeted Ablation of Connexin50 in Mice Results in Microphthalmia and Zonular Pulverulent Cataracts
Thomas W. White,
Thomas W. White
Department of Cell Biology and Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115
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Daniel A. Goodenough,
Daniel A. Goodenough
Department of Cell Biology and Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115
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David L. Paul
David L. Paul
Department of Cell Biology and Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115
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Thomas W. White
Department of Cell Biology and Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115
Daniel A. Goodenough
Department of Cell Biology and Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115
David L. Paul
Department of Cell Biology and Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115
Address correspondence to David L. Paul, Department of Neurobiology, Harvard Medical School, Boston, MA 02115. Tel.: (617) 432-1203. Fax: (617) 432-2955. E-mail: [email protected]
Received:
April 27 1998
Revision Received:
September 10 1998
Online ISSN: 1540-8140
Print ISSN: 0021-9525
1998
J Cell Biol (1998) 143 (3): 815–825.
Article history
Received:
April 27 1998
Revision Received:
September 10 1998
Citation
Thomas W. White, Daniel A. Goodenough, David L. Paul; Targeted Ablation of Connexin50 in Mice Results in Microphthalmia and Zonular Pulverulent Cataracts . J Cell Biol 2 November 1998; 143 (3): 815–825. doi: https://doi.org/10.1083/jcb.143.3.815
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