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Normal development of preimplantation mouse embryos deficient in gap junctional coupling
P A De Sousa1, S C Juneja, S Caveney
1Department of Physiology, The University of Western Ontario, London, Canada.
Journal of Cell Science
|August 1, 1997
Summary
Connexin43 is not essential for early mouse development. Other connexins, like connexin45, compensate for connexin43, ensuring normal embryonic development through gap junctional intercellular communication.
Area of Science:
- Developmental Biology
- Cell Biology
- Molecular Biology
Background:
- Gap junctional intercellular coupling is crucial for preimplantation mouse embryo development.
- Connexin43 (Cx43) is known to form gap junctions during compaction, but its absence does not prevent normal development until implantation.
Purpose of the Study:
- To investigate the compensatory roles of other connexins in early mouse embryonic development.
- To understand the contribution of connexins other than Cx43 to gap junction formation and function.
Main Methods:
- Immunogold electron microscopy to analyze gap junction composition.
- Confocal immunofluorescence microscopy to visualize connexin localization.
- Dye coupling assays using different fluorescent tracers (6-carboxyfluorescein and 2',7'-dichlorofluorescein) to assess gap junction permeability.
Main Results:
- Approximately 30% of gap junctions in compacted morulae lack significant Cx43, suggesting the presence of other connexins.
- Connexin45 (Cx45) is assembled into gap junctions during compaction.
- Cx43 null mutant embryos retain dye coupling ability, albeit reduced and with altered permeability, consistent with Cx45 channel characteristics.
Conclusions:
- Preimplantation development in mice can proceed normally despite altered extent and nature of gap junctional coupling.
- Other gap junction channels, such as those formed by Cx45, can fulfill the role of Cx43 in early embryonic development.