Eomesodermin is required for mouse trophoblast development and mesoderm formation

Andreas P. Russ (), Sigrid Wattler, William H. Colledge, Samuel A. J. R. Aparicio, Mark B. L. Carlton, Jonathan J. Pearce, Sheila C. Barton, M. Azim Surani, Kenneth Ryan, Michael C. Nehls, Valerie Wilson and Martin J. Evans
Additional contact information
Andreas P. Russ: Wellcome/CRC Institute for Cancer and Developmental Biology, University of Cambridge
Sigrid Wattler: Niedersächsisches Institut für Peptidforschung
William H. Colledge: University of Cambridge
Samuel A. J. R. Aparicio: Wellcome/CRC Institute for Cancer and Developmental Biology, University of Cambridge
Mark B. L. Carlton: Wellcome/CRC Institute for Cancer and Developmental Biology, University of Cambridge
Jonathan J. Pearce: Wellcome/CRC Institute for Cancer and Developmental Biology, University of Cambridge
Sheila C. Barton: Wellcome/CRC Institute for Cancer and Developmental Biology, University of Cambridge
M. Azim Surani: Wellcome/CRC Institute for Cancer and Developmental Biology, University of Cambridge
Kenneth Ryan: Wellcome/CRC Institute for Cancer and Developmental Biology, University of Cambridge
Michael C. Nehls: Niedersächsisches Institut für Peptidforschung
Valerie Wilson: Centre of Genome Research, University of Edinburgh, Kings Buildings
Martin J. Evans: Wellcome/CRC Institute for Cancer and Developmental Biology, University of Cambridge

Nature, 2000, vol. 404, issue 6773, 95-99

Abstract: Abstract The earliest cell fate decision in the mammalian embryo separates the extra-embryonic trophoblast lineage, which forms the fetal portion of the placenta, from the embryonic cell lineages. The body plan of the embryo proper is established only later at gastrulation, when the pluripotent epiblast gives rise to the germ layers ectoderm, mesoderm and endoderm. Here we show that the T-box gene Eomesodermin1 performs essential functions in both trophoblast development and gastrulation. Mouse embryos lacking Eomesodermin arrest at the blastocyst stage. Mutant trophoectoderm does not differentiate into trophoblast, indicating that Eomesodermin may be required for the development of trophoblast stem cells2. In the embryo proper, Eomesodermin is essential for mesoderm formation. Although the specification of the anterior–posterior axis and the initial response to mesoderm-inducing signals is intact in mutant epiblasts, the prospective mesodermal cells are not recruited into the primitive streak. Our results indicate that Eomesodermin defines a conserved molecular pathway controlling the morphogenetic movements of germ layer formation and has acquired a new function in mammals in the differentiation of trophoblast.

Date: 2000
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DOI: 10.1038/35003601

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