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Vol. 11, Issue 7, 2459-2470, July 2000

Sussex Centre for Neuroscience, School of Biological Sciences,
University of Sussex, Brighton, BN1 9QG, United Kingdom
Members of the innexin protein family are structural components of
invertebrate gap junctions and are analogous to vertebrate connexins.
Here we investigate two Drosophila innexin genes,
Dm-inx2 and Dm-inx3 and show that they
are expressed in overlapping domains throughout embryogenesis, most
notably in epidermal cells bordering each segment. We also explore the
gap-junction-forming capabilities of the encoded proteins. In paired
Xenopus oocytes, the injection of Dm-inx2
mRNA results in the formation of voltage-sensitive channels in
only ~ 40% of cell pairs. In contrast, Dm-Inx3 never forms
channels. Crucially, when both mRNAs are coexpressed, functional channels are formed reliably, and the electrophysiological properties of these channels distinguish them from those formed by Dm-Inx2 alone.
We relate these in vitro data to in vivo studies. Ectopic expression of
Dm-inx2 in vivo has limited effects on the viability of
Drosophila, and animals ectopically expressing
Dm-inx3 are unaffected. However, ectopic expression of
both transcripts together severely reduces viability, presumably
because of the formation of inappropriate gap junctions. We conclude
that Dm-Inx2 and Dm-Inx3, which are expressed in overlapping domains
during embryogenesis, can form oligomeric gap-junction channels.
Present
address: Department of Biosciences, University of Kent, Canterbury,
Kent, CT2 7NJ UK.
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