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Before death, Atrxnull embryos exhibit a markedly reduced mitotic index, suggesting a proliferative defect. Although the embryonic compartment of the conceptus appears initially normal, by 7.5 dpc Atrxnull embryos display abnormalities in development of the trophoblast, including a depletion in the population of TGCs surrounding the conceptus and a reduction in the size of the ectoplacental cone, which contains the diploid giant cell precursors [22]. TGCs are highly differentiated, postmitotic cells that ultimately form an epithelial layer at the periphery of the placenta, which interfaces with the maternal cells of the decidua [23]. These highly invasive cells are important for mediating initial invasion of the uterine tissue, but are also involved in remodelling the maternal decidua after implantation and in secreting hormones that regulate fetal and maternal growth [24]. Since Atrxnull embryos appear to implant normally, lethality is likely to arise due to a failure of TGC function later during development."}

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{"project":"2_test","denotations":[{"id":"16628246-6895086-85799762","span":{"begin":532,"end":534},"obj":"6895086"},{"id":"16628246-10873707-85799763","span":{"begin":719,"end":721},"obj":"10873707"},{"id":"16628246-7985020-85799764","span":{"begin":964,"end":966},"obj":"7985020"},{"id":"T47412","span":{"begin":532,"end":534},"obj":"6895086"},{"id":"T89259","span":{"begin":719,"end":721},"obj":"10873707"},{"id":"T98024","span":{"begin":964,"end":966},"obj":"7985020"}],"text":"We show that Atrxnull male mice are not viable and embryos die by around 9.5 dpc. Before death, Atrxnull embryos exhibit a markedly reduced mitotic index, suggesting a proliferative defect. Although the embryonic compartment of the conceptus appears initially normal, by 7.5 dpc Atrxnull embryos display abnormalities in development of the trophoblast, including a depletion in the population of TGCs surrounding the conceptus and a reduction in the size of the ectoplacental cone, which contains the diploid giant cell precursors [22]. TGCs are highly differentiated, postmitotic cells that ultimately form an epithelial layer at the periphery of the placenta, which interfaces with the maternal cells of the decidua [23]. These highly invasive cells are important for mediating initial invasion of the uterine tissue, but are also involved in remodelling the maternal decidua after implantation and in secreting hormones that regulate fetal and maternal growth [24]. Since Atrxnull embryos appear to implant normally, lethality is likely to arise due to a failure of TGC function later during development."}

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