Manipulation of gap junctional communication during compaction of the mouse early embryo.
Three treatments that prevent cell flattening during compaction of the mouse preimplantation embryo were assessed for their effects on the onset of gap junctional communication. Medium low in calcium (LCM) and an antiserum to an embryonal carcinoma cell line (anti-EC; Johnson et al. 1979) both prevented the establishment of coupling between blastomeres of the 8-cell embryo as assessed by transmission of carboxyfluorescein or by ionic coupling. Since neither of these agents prevents the contact-mediated induction of cell polarity that occurs at this stage, it is concluded that the induction of this process is not signalled via gap junctions. A monoclonal antibody (ECCD-1; Yoshida-Noro, Suzuki & Takeichi, 1984), that recognizes more specific components of the calcium-dependent cell adhesion system, failed to prevent the onset of junctional coupling. This suggests that the onset of junctional coupling is not dependent upon extensive cell apposition and that the requirement for extracellular Ca2+ resides at a level other than that of cell adhesion. Moreover, neither LCM nor anti-EC could reverse cell coupling once it had become established despite their complete reversal of cell flattening.
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D000818:Animals; D000911:Antibodies, Monoclonal; D001757:Blastomeres / Q000187:drug effects; D002118:Calcium / Q000494:pharmacology; D002450:Cell Communication / Q000187:drug effects*; D003470:Culture Media; D004594:Electrophysiology; D047108:Embryonic Development / Q000187:drug effects*; D005260:Female; D007106:Immune Sera / Q000494:pharmacology; D007365:Intercellular Junctions / Q000187:drug effects* / Q000276:immunology / Q000502:physiology; D051379:Mice; D010781:Photography; D011247:Pregnancy
D000911:Antibodies, Monoclonal; D003470:Culture Media; D007106:Immune Sera; D002118:Calcium