Innexin Gap Junctions

A link between innexin-mediated and ligand/receptor-mediated intercellular signalling

Transgenic innexin-induced lateral inhibition phenotype

Image showing lateral inhibition-like phenotype due to inx7 overexpression

Figure legend: Phenotypes that have previously been associated with aberrant ligand/receptor pathways can be induced by genetically manipulating innexins. The upper left panel shows a photo of the dorsal surface of a Drosophila thorax in a fly that over-expressed Inx7 during development. The focus is on the large bristle sockets (arrow) which are represented as black dots in the lower panels. In wild type flies the sockets are distributed (roughly) evenly over the thoracic surface (right image panels) due to a developmental process called lateral inhibition mediated by the Notch pathway. Over-expression of Inx7 appears to disrupt lateral inhibition suggesting a possible link between gap junction signalling and Notch ligand/receptor signalling.

Image showing that Notch pathway molecules can be downregulated by innexin overexpression

Figure legend: Transgenic expression of Ogre in developing tissues suppresses the expression of Notch pathway genes. The reporter construct E(spl)mβ 1.5 lacZ drives β-galactosidase expression (blue) in a pattern reflecting the expression of endogenous E(spl)mβ protein (Cooper et al. 2000). The transcription factor E(spl)mβ is a downstream target of the Notch pathway in leg discs and abnormal read-out (levels of blue staining) from this reporter can indicate aberrant Notch pathway signalling. The leg discs in A,B and C express this reporter construct. A+B, Notch signalling appears to be normal in control genotype animals, Dll-GAL4 (A) and UAS-ogre (B) - normal levels of blue staining are detected. C, In animals containing both Dll-GAL4 and UAS-ogre, over-expression of Ogre protein causes a notable decrease in expression of the reporter E(spl)mβ 1.5 lacZ.

Cross-talk between gap junction- and ligand/receptor-mediated intercellular signalling pathways have been reported in the published literature for connexin- and innexin-based gap junctions (Lechner et al. 2007, Hirschi et al. 2003). This relationship suggests that these cell-cell communication pathways do not function in isolation. Both are required to coordinate development and disruption of either one can lead to developmental consequences. Relatively little work has been published addressing whether the severity of developmental abnormalities are enhanced (...or not...) in animals possessing defects in both pathways. The availability of innexin and ligand/receptor pathway mutants in Drosophila would facilitate such an investigation.

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