Innexin gap junction subunits co-localise II
Figure legend: Inx2 protein is essential for normal Inx3 subcellular distribution (described here). The panels above-right show a close-up region of the embryo gut corresponding to the region of the white outlined box on the left panel. This gut region is shown for a wild type embryo in the upper panel and for an inx2F43 null mutant in the lower panel. In all cases the embryos were expressing cytoplasmic GFP (green) driven by twist-GAL4 in the anterior region of the gut and they were antibody stained to detect Inx3 protein (red). The wild type has Inx3 plaques throughout the gut (arrows). In the inx2null mutant gut, Inx3 is dispersed over the plasma membrane of the posterior cells (large arrowhead). In addition to GFP this embryo is also expressing UAS-inx2 under the transcriptional control of twistGAL4. So, all cells in this inx2F43/Y mutant that express GFP (green) are also expressing normal Inx2 protein. Comparing the anterior and posterior gut of the mutant (lower panel) one can see that the re-introduction of Inx2 into the anterior gut cells has rescued the ability of Inx3 to form plaques.
Figure legend: What happens to gap junctions when a subunit that should be present is absent from the cell? As shown in the images at the top of this page, the loss of Inx2 results in the failure of Inx3 to aggregate into plaques. However, Inx3 still appears to be synthesised and transported to the plasma membrane where it disperses over the cell surface (Images: Inx3 distribution in Inx2null and Inx2TA181 mutant embryos). With these observations in mind, the diagrams above (based on the Diagram of a gap junction plaque) illustrate four possible outcomes of innexin subunit loss at the molecular level. A, Gap junction channels could completely fail to form even though functional subunits are still expressed in the cell. Cells would fail to couple. B, Remaining subunits manage to form hemichannels in the cell membrane which may/or may not be permeable, but they are not competent to dock with cognate hemichannels on neighbouring cells. This could result in uncoupled, leaky cells. C, Remaining subunits can form hemichannels that are capable of docking to create functional holochannels. But loss of the ability to cluster into structurally stable plaques would presumably make the cells poorly coupled. D, Other gap junction subunits remaining in the cell may be able to form channels capable of coupling cells. It cannot be assumed that the absence of one subunit and/or aberrant positioning of other interacting subunits means that cells will become uncoupled.