Failure of blood-island formation and vasculogenesis in Flk-1-deficient mice
The generation of mice deficient in Flk-1 by disruption of the gene using homologous recombination in embryonic stem (ES) cells is reported, indicating that FlK-1 is essential for yolk-sac blood-island formation and vasculogenesis in the mouse embryo.
Promotion of trophoblast stem cell proliferation by FGF4.
A culture of mouse blastocysts or early postimplantation trophoblasts in the presence of fibroblast growth factor 4 (FGF4) permitted the isolation of permanent trophoblast stem cell lines that exclusively contributed to the trophoplast lineage in vivo in chimeras.
Early lineage segregation between epiblast and primitive endoderm in mouse blastocysts through the Grb2-MAPK pathway.
Interaction between Oct3/4 and Cdx2 Determines Trophectoderm Differentiation
Derivation of completely cell culture-derived mice from early-passage embryonic stem cells.
- A. Nagy, J. Rossant, R. Nagy, W. Abramow-Newerly, J. Roder
- BiologyProceedings of the National Academy of Sciences…
- 15 September 1993
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.
Cdx2 is required for correct cell fate specification and differentiation of trophectoderm in the mouse blastocyst
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.
The Hippo signaling pathway components Lats and Yap pattern Tead4 activity to distinguish mouse trophectoderm from inner cell mass.
Role of the Flt-1 receptor tyrosine kinase in regulating the assembly of vascular endothelium
It is reported that Flt-1 is essential for the organization of embryonic vasculature, but is not essential for endothelial cell differentiation, and it is suggested that the FlT-1 signalling pathway may regulate normal endothelium cell-cell or cell-matrix interactions during vascular development.
Retinoid Signaling Determines Germ Cell Fate in Mice
It is found that retinoic acid, produced by mesonephroi of both sexes, causes germ cells in the ovary to enter meiosis and inititate oogenesis, and precise regulation of retinoid levels during fetal gonad development provides the molecular control mechanism that specifies germ cell fate.
Expression of a retinoic acid response element-hsplacZ transgene defines specific domains of transcriptional activity during mouse embryogenesis.
It is shown that a RA response element (RARE) present in the RAR beta gene can direct specific spatial and temporal expression of an hsplacZ transgene during mouse embryogenesis, suggesting that, in vivo, some of the morphogenetic effects of RA could be mediated through localized transcriptional activity controlled by the various RARs.