Abstract
ANTERIOR-POSTERIOR (A–P) patterning is of fundamental importance throughout vertebrate embryonic development. Murine members of the trithorax (trx) and Polycomb group (Pc-G) of genes regulate A–P patterning of segmented axial structures1–4, demonstrating conserved upstream regulation of homeotic pathways between Drosophila and mouse. Here we report the positional cloning of a classical mouse mutation, eed (for embryonic ectoderm development), which is the highly conserved homologue of the Drosophila Pc-G gene esc (for extra sex combs), a long-term represser of homeotic genes5. Mutants homozygous for a null allele of eed display disrupted A–P patterning of the primitive streak during gastrulation. Mutant embryos lack a node, noto-chord and somites, and there is no neural induction6. In contrast to absence of anterior structures, extra-embryonic mesoderm is abundant. Mice carrying a hypomorphic eed mutation exhibit posterior transformations along the axial skeleton. These results indicate that eed is required globally for A–P patterning throughout embryogenesis.
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Schumacher, A., Faust, C. & Magnuson, T. Positional cloning of a global regulator of anterior–posterior patterning in mice. Nature 383, 250–253 (1996). https://doi.org/10.1038/383250a0
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DOI: https://doi.org/10.1038/383250a0
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