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Journal ArticleDOI

Placental development: Lessons from mouse mutants

TLDR
Current studies of mouse mutants with disrupted placental development indicate that signalling interactions between the placental trophoblast and embryonic cells have a key role in placental morphogenesis, which should provide novel insights into human placental function.
Abstract
The placenta is the first organ to form during mammalian embryogenesis. Problems in its formation and function underlie many aspects of early pregnancy loss and pregnancy complications in humans. Because the placenta is critical for survival, it is very sensitive to genetic disruption, as reflected by the ever-increasing list of targeted mouse mutations that cause placental defects. Recent studies of mouse mutants with disrupted placental development indicate that signalling interactions between the placental trophoblast and embryonic cells have a key role in placental morphogenesis. Furthering our understanding of mouse trophoblast development should provide novel insights into human placental function.

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Journal ArticleDOI

Initial sequencing and comparative analysis of the mouse genome.

Robert H. Waterston, +222 more
- 05 Dec 2002 - 
TL;DR: The results of an international collaboration to produce a high-quality draft sequence of the mouse genome are reported and an initial comparative analysis of the Mouse and human genomes is presented, describing some of the insights that can be gleaned from the two sequences.
Journal ArticleDOI

Multipotent cell lineages in early mouse development depend on SOX2 function

TL;DR: The data suggest that maternal components could be involved in establishing early cell fate decisions and that a combinatorial code, requiring SOX2 and OCT4, specifies the first three lineages present at implantation.
Journal ArticleDOI

Interaction between Oct3/4 and Cdx2 Determines Trophectoderm Differentiation

TL;DR: It is shown that the differentiation of TE cells can be mimicked by overexpression of Caudal-related homeobox 2 (Cdx2), which is sufficient to generate proper trophoblast stem (TS) cells and suggests that reciprocal inhibition between lineage-specific transcription factors might be involved in the first differentiation event of mammalian development.
Journal ArticleDOI

Natural killer cells and pregnancy.

TL;DR: No convincing evidence of uterine maternal T-cell recognition of placental trophoblast cells has been found, but instead, there might be maternal allorecognition mediated by uterine natural killer cells that recognize unusual fetal trophOBlast MHC ligands.
Journal ArticleDOI

Cdx2 is required for correct cell fate specification and differentiation of trophectoderm in the mouse blastocyst

TL;DR: Cdx2 is essential for segregation of the ICM and TE lineages at the blastocyst stage by ensuring repression of Oct4 and Nanog in the TE.
References
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Journal ArticleDOI

Targeted mutation of the DNA methyltransferase gene results in embryonic lethality.

TL;DR: Results indicate that while a 3-fold reduction in levels of genomic m5C has no detectable effect on the viability or proliferation of ES cells in culture, a similar reduction of DNA methylation in embryos causes abnormal development and embryonic lethality.
Journal ArticleDOI

Formation of Pluripotent Stem Cells in the Mammalian Embryo Depends on the POU Transcription Factor Oct4

TL;DR: It is reported that the activity of Oct4 is essential for the identity of the pluripotential founder cell population in the mammalian embryo and also determines paracrine growth factor signaling from stem cells to the trophectoderm.
Journal ArticleDOI

Derivation of completely cell culture-derived mice from early-passage embryonic stem cells

TL;DR: Fully potent early passage R1 cells and the R1-S3 subclone should be very useful not only for ES cell-based genetic manipulations but also in defining optimal in vitro culture conditions for retaining the initial totipotency of ES cells.
Journal ArticleDOI

PPAR gamma is required for placental, cardiac, and adipose tissue development.

TL;DR: Findings both confirm and expand the current known spectrum of physiological functions regulated by PPAR gamma, implicating a previously unrecognized dependence of the developing heart on a functional placenta.
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