Innexins are detected at all developmental stages in salivary glands throughout the life of Drosophila. When glands of similar size, but different developmental stage (eg. larval vs. pupal), are stained side-by-side to detect an innexin protein it becomes apparent that there is a massive difference in the protein level in each developmental stage. Hypothetically, gap junctions may play a role in synchronizing the release of glue vesicles in a coordinated fashion from salivary glands near the end of the larval stage. So why would innexin protein levels increase so significantly after this stage when there is nothing left for these cells to do except enter the apoptotic pathway and disintegrate?
- - Gap junctions might be important for coordinating entry into the apoptototic pathway. Ensuring that all cells of the gland are switched to auto-destruct at the same time. But if a lower amount of innexins successfully coordinate glue release (...if they have any role in that process)...why would so much more protein be required to coordinate apoptosis?
- - Do innexins play an important role in the actual process of apoptosis (at least in salivary gland cells)?
- - Why do putative annular junctions accumulate at the basal end of pupal cells instead of being broken down by the lysosomal and proteasomal pathways? Do these large vesicles have role in apoptosis?
- - Is any of the innexin in the pupal salivary gland present as regulated hemichannels? - synchronised opening of such channels and the rapid influx of ions after initiation of the auto-destruct signal would have a significant impact in mediating cell death.
- - Do larger molecules such as proteins pass through gap junctions during the pupal stage? After all, there's no published evidence suggesting that all innexin-based channels have similar pore sizes (we don't even know if they're generally constructed from six subunits, like connexins, Diagram of gap junction channels). There are reports of large molecules passing through insect gap junctions (Brooks and Woodruff, 2004).