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Mutation of the alpha3 connexin gene in mice did not affect the initial formation of lenses and lens fiber differentiation but caused proteolytic degradation of crystallins in mice with a double dose of the mutant gene. This led to the development of nuclear cataracts. These results reveal the importance of gap junctions in the maintenance of lens transparency. Gap junctions are the means of adjacent cell to communicate with one another and may function as a structural component in cellular organization.

Cell communication is essential to maintain the organization of cells. It coordinates cellular activities while at the same time, lets cells retain their individuality. Direct cell-cell contact is achieved via specialized cell surface membrane structures called gap junctions. Gap junctions are made up of a family of proteins called connexins which define the properties of gap junction channels such as permeability to molecules and voltage sensitivity.

Laser scanning confocal microscopic analysis of epidermal gap junctions reveals that gap junctions are present as junctional plaques that composed of alpha(1) and beta(2) connexins during the embryonic development. Beta(2) connexin is selectively expressed in the upper and granular differentiated spinous layers. Alpha(1) is detected in the developing basal layer and less differentiated spinous layer. The segregated domains of both connexins encode a single homooligomer protein.