Lens gap junctions: a structural hypothesis for nonregulated low-resistance intercellular pathways.

Abstract

Structural evidence is presented which suggests that gap junctions between lens fibers are adapted to remain in a low-resistance physiological state, under conditions which switch gap junctions in other tissues to a high-resistance state. The lens gap junction subunits (connexons) do not crystallize in the membrane plane in response to fixation, anoxia, lens damage, or homogenization and isolation. Rapid freezing experiments (Raviola et al.) suggest connexon resistance. Freshly homogenized liver cytoplasm does not contain an assayable factor which can crystallize connexons in lens gap junctions. Polyacrylamide gel electrophoresis of enrighed preparations of isolated lens junctions reveals a 27 +/- 2 kilodalton principal polypeptide which is similar in electrophoretic mobility to one of the principal polypeptides resolved in gels of isolated hepatocyte gap junctions. These results indicate that the whole lens may be extremely vulnerable to surface injury, perhaps even to injury of a single lens fiber.