LENS GAP-JUNCTIONS - STRUCTURAL HYPOTHESIS FOR NON-REGULATED LOW-RESISTANCE INTER-CELLULAR PATHWAYS

Abstract

From experiments with calf eyes and mouse and chicken lenses structural evidence was presented suggesting gap junctions between lens fibers were 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) did not crystallize in the membrane plane in respone to fixation, anoxia, lens damage or homogenization and isolation. Rapid freezing experiments (Raviola) suggest connexon crystallization in other nonlens tissues was a morphological consequence of the switch to high resistance. Freshly homogenized liver cytoplasm did not contain an assayable factor for crystallizing connexons in lens gap junctions. Polyacrylamide gel electrophoresis of enriched preparations of isolated lens junctions revealed a 27 .+-. 2 kdalton principal polypeptide similar in electrophoretic mobility to 1 of the principal polypeptides resolved in gels of isolated hepatocyte gap junctions. The whole lens apparently was extremely vulnerable to surface injury, perhaps even to injury of a single lens fiber.