Possible regulation of connexin function through gene duplication events

Abstract

Gap junctions are proteinaceous channels that allow direct cell–cell communication via the exchange of small molecules and ions among neighboring cells. The subunits of gap junction channels found in chordates are termed connexins. Remarkably, a large number of connexin genes have been identified in all vertebrate species examined to date. It is not fully understood why so many connexin genes are required for what appears to be a simple function. Phylogenetic analyses have revealed connexin losses and gains during evolution. Presently, it is of interest to clarify why so many connexin genes are retained within genomes. One possibility is that additional connexins provide novel coupling properties for gap junction channels. Alternatively, connexin genes may be capable of establishing novel functions in order to regulate their paralogous connexin, which retains a more typical gap junction activity. Two examples of the latter have been identified. Both mouse Cx33 and zebrafish Cx40.8 can be found intracellularly, and both are implicated in the regulation of Cx43‐based gap junctional communication. Continuing studies will provide mechanistic details into how these non‐gap junction channel connexins regulate the function of gap junction channels. WIREs Membr Transp Signal 2013, 2:221–225. doi: 10.1002/wmts.92Conflict of interest: The author has declared no conflicts of interest for this article.For further resources related to this article, please visit the WIREs website.