Cell and tissue requirements for the gene eed during mouse gastrulation and organogenesis.
Mouse embryos homozygous for the allele eed(l7Rn5-3354SB) of the Polycomb Group gene embryonic ectoderm development (eed) display a gastrulation defect in which epiblast cells move through the streak and form extraembryonic mesoderm derivatives at the expense of development of the embryo proper. Here we demonstrate that homozygous mutant ES cells have the capacity to differentiate embryonic cell types both in vitro as embryoid bodies and in vivo as chimeric embryos. In chimeric embryos, eed mutant cells can respond to wild-type signals and participate in normal gastrulation movements. These results indicate a non-cell-autonomous function for eed. Evidence of mutant cell exclusion from the forebrain and segregation within somites, however, suggests that eed has cell-autonomous roles in aspects of organogenesis. A requirement for eed in the epiblast during embryonic development is supported by the fact that high-contribution chimeras could not be rescued by a wild-type extraembryonic environment.[1]References
- Cell and tissue requirements for the gene eed during mouse gastrulation and organogenesis. Morin-Kensicki, E.M., Faust, C., LaMantia, C., Magnuson, T. Genesis (2001) [Pubmed]
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