ArticleDevelopmental biology2015
Nodal signaling from the visceral endoderm is required to maintain Nodal gene expression in the epiblast and drive DVE/AVE migration.
Article in Developmental biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 38 citations in OpenAlex.
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- Induction of Rosette-to-Lumen stage embryoids using reprogramming paradigms in ESCs.Nature communications · 2021Article
- A single cell characterisation of human embryogenesis identifies pluripotency transitions and putative anterior hypoblast centre.Nature communications · 2021Article
- Mouse gastrulation: Coordination of tissue patterning, specification and diversification of cell fate.Mechanisms of development · 2020Review
- Implantation initiation of self-assembled embryo-like structures generated using three types of mouse blastocyst-derived stem cells.Nature communications · 2019Article
- JAM-A overexpression is related to disease progression in diffuse large B-cell lymphoma and downregulated by lenalidomide.Scientific reports · 2017Article
- Ino80 is essential for proximal-distal axis asymmetry in part by regulating Bmp4 expression.BMC biology · 2016Article
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Authors and funding
7 authors at 5 institutions in 2 countries.
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Abstract
In the early mouse embryo, a specialized population of extraembryonic visceral endoderm (VE) cells called the distal VE (DVE) arises at the tip of the egg cylinder stage embryo and then asymmetrically migrates to the prospective anterior, recruiting additional distal cells. Upon migration these cells, called the anterior VE (AVE), establish the anterior posterior (AP) axis by restricting gastrulation-inducing signals to the opposite pole. The Nodal-signaling pathway has been shown to have a critical role in the generation and migration of the DVE/AVE. The Nodal gene is expressed in both the VE and in the pluripotent epiblast, which gives rise to the germ layers. Previous findings have provided conflicting evidence as to the relative importance of Nodal signaling from the epiblast vs. VE for AP patterning. Here we show that conditional mutagenesis of the Nodal gene specifically within the VE leads to reduced Nodal expression levels in the epiblast and incomplete or failed DVE/AVE migration. These results support a required role for VE Nodal to maintain normal levels of expression in the epiblast, and suggest signaling from both VE and epiblast is important for DVE/AVE migration.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.