Innexins get into the gap.
Connexins were first identified in the 1970s as the molecular components of vertebrate gap junctions. Since then a large literature has accumulated on the cell and molecular biology of this multi-gene family culminating recently in the findings that connexin mutations are implicated in a variety of human diseases. Over two decades, the terms "connexin" and "gap junction" had become almost synonymous. In the last few years a second family of gap-junction genes, the innexins, has emerged. These have been shown to form intercellular channels in genetically tractable invertebrate organisms such as Drosophila melanogaster and Caenorhabditis elegans. The completed genomic sequences for the fly and worm allow identification of the full complement of innexin genes in these two organisms and provide valuable resources for genetic analyses of gap junction function.
Phelan
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P
Department of Biosciences, University of Kent, Canterbury CT2 7NJ, UK. P.Phelan@ukc.ac.uk
Starich
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TA
D000818:Animals; D017173:Caenorhabditis elegans / Q000235:genetics / Q000502:physiology; D017630:Connexins / Q000235:genetics / Q000502:physiology*; D004331:Drosophila melanogaster / Q000235:genetics / Q000502:physiology; D017629:Gap Junctions / Q000502:physiology*; D017238:Genes, Helminth; D017344:Genes, Insect; D006801:Humans; D007448:Invertebrates; D007473:Ion Channels / Q000235:genetics / Q000502:physiology; D009154:Mutation
D017630:Connexins; D007473:Ion Channels