Distinct effects of ectopic expression of Wnt-1, activin B, and bFGF on gap junctional permeability in 32-cell Xenopus embryos.
A polarity in gap junctional permeability normally exists in 32-cell stage Xenopus embryos, in that dorsal cells are relatively more coupled than ventral cells, as measured by transfer of Lucifer yellow dye. The current study extends our analysis of whether gap junctional permeability at this stage can be modulated by secreted factors, and whether the polarity in gap junctional permeability correlates with the effects of ectopic expression of these secreted factors on the subsequent phenotype of the developing embryo. Following ectopic expression of activin B or Wnt-1, but not bFGF, the transfer of Lucifer yellow between ventral animal pole cells is detected in a greater percentage of 32-cell stage embryos. This increased incidence of dye transfer between ventral cells correlates with axial duplications later in development. However, there are differences in the extent of Lucifer yellow transfer between animal and vegetal hemisphere blastomeres which is dependent on whether activin B or Wnt-1 RNA had previously been injected. These results suggest that enhanced gap junctional permeability between ventral cells of 32-cell Xenopus embryos correlates with subsequent defects in the dorsoventral axis, although there are at present no direct data demonstrating a role for gap junctions in establishment or maintenance of this axis. Moreover, while both activin B and bFGF are mesoderm-inducing growth factors, only activin B has effects on gap junctional permeability in 32-cell embryos following ectopic expression, demonstrating an interesting difference in physiological responses to expression of these factors.
Olson
D J
DJ
Department of Pharmacology, University of Washington School of Medicine, Seattle 98195.
Moon
R T
RT
D028341:Activins; D000818:Animals; D016222:Fibroblast Growth Factor 2 / Q000494:pharmacology*; D015870:Gene Expression; D007365:Intercellular Junctions / Q000187:drug effects*; D009842:Oligopeptides; D010455:Peptides / Q000494:pharmacology*; D011518:Proto-Oncogene Proteins / Q000494:pharmacology*; D015398:Signal Transduction; D051153:Wnt Proteins; D051155:Wnt1 Protein; D029867:Xenopus Proteins; D014982:Xenopus laevis / Q000196:embryology; D029961:Zebrafish Proteins
D009842:Oligopeptides; D010455:Peptides; D011518:Proto-Oncogene Proteins; C495249:WNT1 protein, Xenopus; D051153:Wnt Proteins; D051155:Wnt1 Protein; D029867:Xenopus Proteins; D029961:Zebrafish Proteins; C044147:activin B; D016222:Fibroblast Growth Factor 2; D028341:Activins; C048617:myelopeptides