ArticleDevelopmental cell2024
An integrated approach identifies the molecular underpinnings of murine anterior visceral endoderm migration.
Article in Developmental cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Discovering the unexpected: Insights into the dynamics of mouse neural tube closure revealed by time-lapse imaging.Developmental biology · 2026Review
- Self-organization of mouse embryonic stem cells into reproducible pre-gastrulation embryo models via CRISPRa programming.Cell stem cell · 2025Article
- Differentiation success of reprogrammed cells is heterogeneous in vivo and modulated by somatic cell identity memory.Stem cell reports · 2025Article
- Origin, fate and function of extraembryonic tissues during mammalian development.Nature reviews. Molecular cell biology · 2025Review
- Tissue-intrinsic beta-catenin signals antagonize Nodal-driven anterior visceral endoderm differentiation.Nature communications · 2024Article
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Authors and funding
12 authors.
Funding
Abstract
The anterior visceral endoderm (AVE) differs from the surrounding visceral endoderm (VE) in its migratory behavior and ability to restrict primitive streak formation to the opposite side of the mouse embryo. To characterize the molecular bases for the unique properties of the AVE, we combined single-cell RNA sequencing of the VE prior to and during AVE migration with phosphoproteomics, high-resolution live-imaging, and short-term lineage labeling and intervention. This identified the transient nature of the AVE with attenuation of "anteriorizing" gene expression as cells migrate and the emergence of heterogeneities in transcriptional states relative to the AVE's position. Using cell communication analysis, we identified the requirement of semaphorin signaling for normal AVE migration. Lattice light-sheet microscopy showed that Sema6D mutants have abnormalities in basal projections and migration speed. These findings point to a tight coupling between transcriptional state and position of the AVE and identify molecular controllers of AVE migration.
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