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The development of XO gynogenetic mouse embryos
1MRC Mammalian Development Unit, University College London, UK.
Development (Cambridge, England)
|March 1, 1987
Summary
Diploid gynogenetic embryos die due to the absence of paternal chromosomes, not X chromosome inactivation issues. This study reveals that lacking a paternal autosome set is sufficient to cause embryo inviability.
Area of Science:
- Developmental Biology
- Genetics
- Reproductive Biology
Background:
- Diploid gynogenetic embryos (two maternal sets, no paternal) die near implantation.
- Normal females inactivate paternal X chromosomes in extraembryonic membranes.
- Gynogenetic inviability may stem from X chromosome inactivation challenges.
Purpose of the Study:
- To investigate the cause of diploid gynogenetic embryo inviability.
- To determine if X chromosome inactivation is the primary factor.
- To explore the role of paternal genetic contribution in embryonic development.
Main Methods:
- Construction of XO gynogenetic embryos via nuclear transplantation at the 1-cell stage.
- Comparison of mortality rates between XX and XO gynogenetic embryos.
- Analysis of embryonic survival around implantation.
Main Results:
- XO gynogenetic embryos exhibited mortality similar to XX gynogenetic counterparts.
- The absence of a paternally derived X chromosome did not alter survival rates.
- Embryo inviability is linked to the lack of paternal autosomes, not X chromosome issues.
Conclusions:
- The inviability of gynogenetic embryos is primarily due to the absence of paternal autosomes.
- X chromosome inactivation is not the critical factor for survival at this stage.
- Findings suggest a crucial role for autosomal imprinting in early embryonic development.