Affordable Access

deepdyve-link
Publisher Website

Vg1-Nodal heterodimers are the endogenous inducers of mesendoderm.

Authors
  • Montague, Tessa G1
  • Schier, Alexander F1, 2, 3, 4, 5
  • 1 Department of Molecular and Cellular Biology, Harvard University, Cambridge, United States. , (United States)
  • 2 Center for Brain Science, Harvard University, Cambridge, United States. , (United States)
  • 3 Broad Institute of MIT and Harvard, Cambridge, United States. , (United States)
  • 4 Harvard Stem Cell Institute, Cambridge, United States. , (United States)
  • 5 FAS Center for Systems Biology, Harvard University, Cambridge, United States. , (United States)
Type
Published Article
Journal
eLife
Publisher
"eLife Sciences Organisation, Ltd."
Publication Date
Nov 15, 2017
Volume
6
Identifiers
DOI: 10.7554/eLife.28183
PMID: 29140251
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Nodal is considered the key inducer of mesendoderm in vertebrate embryos and embryonic stem cells. Other TGF-beta-related signals, such as Vg1/Dvr1/Gdf3, have also been implicated in this process but their roles have been unclear or controversial. Here we report that zebrafish embryos without maternally provided vg1 fail to form endoderm and head and trunk mesoderm, and closely resemble nodal loss-of-function mutants. Although Nodal is processed and secreted without Vg1, it requires Vg1 for its endogenous activity. Conversely, Vg1 is unprocessed and resides in the endoplasmic reticulum without Nodal, and is only secreted, processed and active in the presence of Nodal. Co-expression of Nodal and Vg1 results in heterodimer formation and mesendoderm induction. Thus, mesendoderm induction relies on the combination of two TGF-beta-related signals: maternal and ubiquitous Vg1, and zygotic and localized Nodal. Modeling reveals that the pool of maternal Vg1 enables rapid signaling at low concentrations of zygotic Nodal.

Report this publication

Statistics

Seen <100 times