Innexins and dorsal closure - a model for studying gap junctions and wound healing?
A projection of Z-series images showing the distribution of Inx2 protein (blue) in epidermal cells of a 10-12 hour old, wild type embryo. The embryo has also been antibody-stained to detect fasciclinIII (red), an adhesion molecule located on cell plasma membranes. A, Arrowheads indicate where leading edge cells are about to join at the dorsal surface midline of the embryo (at the Gap). B, Arrowheads indicate where leading edge cells have just joined the two epidermal sheets. Inx2 protein distribution does not look any different in leading edge cells than in other cells of the epidermis. No aspect of the protein distribution suggests that there may be a role for Inx2 in dorsal closure (no increased Inx2 accumulation at the leading edge, for example). Also, inx2 mutants do not exhibit any dorsal closure phenotype. It is possible that maternally contributed, normal, innexin protein could mask such a phenotype in mutants, and intriguingly, embryos that lack the maternally inherited component of inx2 mRNA but possess a single zygotic copy (Bauer et al, 2004) can exhibit a large hole in the cuticle that grossly resembles the cuticular phenotypes observed in dorsal closure mutants (a list of such mutants can be found in a review by Martin et al, 2004). Hopefully, further analysis of this phenotype will reveal whether inx2, or indeed any of the other innexin family members, are required for dorsal closure. Possibly then, the dorsal closure model of wound healing might provide insights into the reported role of connexin-based gap junctions and wound healing (Chanson et al. 2005).