This article is a US Government work and, as such, is in the public domain in the United States of America.
Patterns & Phenotypes
The DVE changes distal epiblast fate from definitive endoderm to neurectoderm by antagonizing nodal signaling†
Article first published online: 30 APR 2007
Published 2007 Wiley-Liss, Inc.
Special Issue: Special Focus on Segmentation
Volume 236, Issue 6, pages 1602–1610, June 2007
How to Cite
Miura, S. and Mishina, Y. (2007), The DVE changes distal epiblast fate from definitive endoderm to neurectoderm by antagonizing nodal signaling. Dev. Dyn., 236: 1602–1610. doi: 10.1002/dvdy.21166
- Issue published online: 16 MAY 2007
- Article first published online: 30 APR 2007
- Manuscript Accepted: 19 MAR 2007
- Intramural Research Program of the NIH
- National Institute of Environmental Health Science
- embryo culture;
- distal epiblast, neuroectoderm;
- definitive endoderm
To assess the function of the distal visceral endoderm (DVE) of embryonic day 5.5 (E5.5) embryos, we established a system to directly ablate the DVE and observe the consequences after culture. When the DVE was successfully ablated, such embryos (DVE-ablated embryos) showed deregulated expression of Nodal and Wnt3 and ectopically formed the primitive streak at the proximal portion of the embryo. The DVE and anterior visceral endoderm (AVE) are implicated in the development of neurectoderm. We found that the distal epiblast of E5.5 embryo rotates anteriorly by the beginning of gastrulation. These cells remained to be anteriorly located during gastrulation and contributed to the ectoderm in the anterior side of the embryo. This indicates that the distal epiblast of E5.5 embryo becomes neurectoderm in normal development. In DVE-ablated embryos, the distal epiblast did not show any movement during culture and was abnormally fated to early definitive endoderm lineage. The data suggest that down-regulation of Nodal signaling in the distal epiblast of E5.5 embryo may be an initial step of neural development. Developmental Dynamics 236:1602–1610, 2007. Published 2007 Wiley-Liss, Inc.