Maternal <i>Cdx2</i> is dispensable for mouse development

Blij, Stephanie; Frum, Tristan; Akyol, Aytekin; Fearon, Eric R.; Ralston, Amy

doi:10.1242/dev.086025

Cited by 52 publications

(51 citation statements)

References 25 publications

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“…In mice, both Cdx2-knockout and -knockdown blastocysts exhibit a hatching failure, decreased cell number, abnormal TE cell junctions/polarity and a disturbed TE GRN (Blij et al, 2012;Jedrusik et al, 2010Jedrusik et al, , 2015Nishioka et al, 2008;Ralston and Rossant, 2008;Strumpf et al, 2005;Wu et al, 2010). In primates (Sritanaudomchai et al, 2009) and cattle (Goissis and Cibelli, 2014;Madeja et al, 2013), CDX2 knockdown results in a hatching failure and deficient cell proliferation in blastocysts.…”

Section: Discussionmentioning

confidence: 99%

“…Several studies have shown that CDX2 is not required for development of the mouse cleavage stage or for apical polarization and viability of mouse TE cells (Blij et al, 2012;Ralston and Rossant, 2008;Strumpf et al, 2005;Wu et al, 2010). These studies demonstrate that mouse embryos depleted of Cdx2 through either gene knockout or RNA interference (RNAi) are able to develop to normal blastocysts in terms of overall cell number, ICM:TE ratio, and TE apical polarity, despite abnormal cell junctions.…”

Section: Cdx2mentioning

confidence: 99%

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CDX2 is essential for cell proliferation and polarity in porcine blastocysts

et al. 2017

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The role of CDX2 in trophectoderm (TE) cells has been extensively studied, yet the results are contradictory and species specific. Here, CDX2 expression and function were explored in early porcine embryos. Notably, siRNA-mediated gene knockdown and lentivirusmediated TE-specific gene regulation demonstrated that CDX2 is essential for the maintenance of blastocyst integrity by regulating the BMP4-mediated blastocyst niche and classic protein kinase C (PKC)-mediated TE polarity in mammalian embryos. Mechanistically, CDX2-depleted porcine embryos stalled at the blastocyst stage and exhibited apoptosis and inactive cell proliferation, possibly resulting from BMP4 downregulation. Moreover, TE cells in CDX2-depleted blastocysts displayed defective F-actin apical organization associated with downregulation of PKCα (PRKCA). Collectively, these results provide further insight into the functional diversity of CDX2 in early mammalian embryos.

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Section: Discussionmentioning

confidence: 99%

Section: Cdx2mentioning

confidence: 99%

CDX2 is essential for cell proliferation and polarity in porcine blastocysts

et al. 2017

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“…The apical localization of Cdx2 mRNA and its asymmetric inheritance by polar cells during asymmetric division is proposed to be involved in establishing TE-specific CDX2 expression (Jedrusik et al, 2010;Jedrusik et al, 2008;Skamagki et al, 2013). Precisely when CDX2 acts, however, remains unclear: some studies suggest that maternal CDX2 is required for proper cell cycle progression and cell survival (Jedrusik et al, 2015); however, a separate study has shown that there is no clear contribution of maternal CDX2 to lineage specification and that maternal CDX2 is dispensable for preimplantation development (Blij et al, 2012). What causes the discrepancy in these two studies is not known, but differences in mouse strains and/ or in vitro embryo culture conditions might have affected their experimental outcomes.…”

Section: Experimental Manipulations and Consequencesmentioning

confidence: 99%

Lineage specification in the mouse preimplantation embryo

2016

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During mouse preimplantation embryo development, totipotent blastomeres generate the first three cell lineages of the embryo: trophectoderm, epiblast and primitive endoderm. In recent years, studies have shown that this process appears to be regulated by differences in cell-cell interactions, gene expression and the microenvironment of individual cells, rather than the active partitioning of maternal determinants. Precisely how these differences first emerge and how they dictate subsequent molecular and cellular behaviours are key questions in the field. As we review here, recent advances in live imaging, computational modelling and single-cell transcriptome analyses are providing new insights into these questions.

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“…At the molecular level, the transcription factor CDX2 is specifically expressed in the TE (derived from outer cells) and is essential for TE formation (Blij et al, 2012;Ralston and Rossant, 2008;Strumpf et al, 2005;Wu et al, 2010). The Hippo/YAP signaling cascade has been shown to control TE-specific CDX2 expression (Cockburn et al, 2013;Hirate et al, 2013;Leung and Zernicka-Goetz, 2013;Nishioka et al, 2009;Sasaki, 2010).…”

Section: Introductionmentioning

confidence: 99%

Initiation of Hippo signaling is linked to polarity rather than to cell position in the pre-implantation mouse embryo

et al. 2014

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In the mouse embryo, asymmetric divisions during the 8-16 cell division generate two cell types, polar and apolar cells, that are allocated to outer and inner positions, respectively. This outer/inner configuration is the first sign of the formation of the first two cell lineages: trophectoderm (TE) and inner cell mass (ICM). Outer polar cells become TE and give rise to the placenta, whereas inner apolar cells become ICM and give rise to the embryo proper and yolk sac. Here, we analyze the frequency of asymmetric divisions during the 8-16 cell division and assess the relationships between cell polarity, cell and nuclear position, and Hippo signaling activation, the pathway that initiates lineage-specific gene expression in 16-cell embryos. Although the frequency of asymmetric divisions varied in each embryo, we found that more than six blastomeres divided asymmetrically in most embryos. Interestingly, many apolar cells in 16-cell embryos were located at outer positions, whereas only one or two apolar cells were located at inner positions. Live imaging analysis showed that outer apolar cells were eventually internalized by surrounding polar cells. Using isolated 8-cell blastomeres, we carefully analyzed the internalization process of apolar cells and found indications of higher cortical tension in apolar cells than in polar cells. Last, we found that apolar cells activate Hippo signaling prior to taking inner positions. Our results suggest that polar and apolar cells have intrinsic differences that establish outer/inner configuration and differentially regulate Hippo signaling to activate lineage-specific gene expression programs.

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Maternal Cdx2 is dispensable for mouse development

Cited by 52 publications

References 25 publications

CDX2 is essential for cell proliferation and polarity in porcine blastocysts

CDX2 is essential for cell proliferation and polarity in porcine blastocysts

Lineage specification in the mouse preimplantation embryo

Initiation of Hippo signaling is linked to polarity rather than to cell position in the pre-implantation mouse embryo

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