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. Author manuscript; available in PMC: 2010 Mar 1.
Published in final edited form as: Exp Eye Res. 2008 Dec 6;88(3):600–609. doi: 10.1016/j.exer.2008.11.024

Fig. 8.

Fig. 8

Proposed mechanism of formation of CX50P88S cytosolic accumulations. CX50P88S is synthesized in the rough endoplasmic reticulum (rER). This mutant protein does not leave the rER compartment or follow the normal pathway of wild type CX50 to the plasma membrane (1). Continuing synthesis of CX50P88S leads to the formation of an out-pocketing from the rER membrane in which the mutant protein becomes concentrated (2). The size of the out-pocketing increases as more CX50P88S protein is synthesized (3). This leads to a highly localized concentration of CX50P88S which provokes the collapse of the ER membrane from opposite sides, displacement of the ER luminal contents, and formation of a sheet-like (gap junction-like) double membrane structure (4). This double membrane structure grows by continued addition of more CX50P88S-containing vesicles (not shown in the diagram) until it reaches a critical size where it folds upon itself to form a tubular structure or nascent accumulation (5).