ArticleeLife2022
Regulation of Nodal signaling propagation by receptor interactions and positive feedback.
Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Fundamental limits on symmetry breaking by Turing-like activator-inhibitor mechanisms.Development (Cambridge, England) · 2026Article
- Tissue rigidity phase transition shapes morphogen gradients.Nature cell biology · 2026Article
- Measuring morphogen transport over multiple spatial scales in live zebrafish embryos.Nature communications · 2026Article
- Recurrent evolution of ligand-binding domain multiplicity fine-tunes TGFβ signaling in vertebrates.Nature communications · 2026Article
- PGC-derived migrasomes couple PGC proliferation with migration.Nature communications · 2026Article
- Myosin1G promotes Nodal signaling to control zebrafish left-right asymmetry.Nature communications · 2024Article
- Gastrulation-stage gene expression inScience advances · 2024Article
- Robust axis elongation by Nodal-dependent restriction of BMP signaling.Development (Cambridge, England) · 2024Article
- Single-molecule tracking of Nodal and Lefty in live zebrafish embryos supports hindered diffusion model.Nature communications · 2022Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During vertebrate embryogenesis, the germ layers are patterned by secreted Nodal signals. In the classical model, Nodals elicit signaling by binding to a complex comprising Type I/II Activin receptors (Acvr) and the co-receptor Tdgf1. However, it is currently unclear whether receptor binding can also affect the distribution of Nodals themselves through the embryo, and it is unknown which of the putative Acvr paralogs mediate Nodal signaling in zebrafish. Here, we characterize three Type I (Acvr1) and four Type II (Acvr2) homologs and show that - except for Acvr1c - all receptor-encoding transcripts are maternally deposited and present during zebrafish embryogenesis. We generated mutants and used them together with combinatorial morpholino knockdown and CRISPR F0 knockout (KO) approaches to assess compound loss-of-function phenotypes. We discovered that the Acvr2 homologs function partly redundantly and partially independently of Nodal to pattern the early zebrafish embryo, whereas the Type I receptors Acvr1b-a and Acvr1b-b redundantly act as major mediators of Nodal signaling. By combining quantitative analyses with expression manipulations, we found that feedback-regulated Type I receptors and co-receptors can directly influence the diffusion and distribution of Nodals, providing a mechanism for the spatial restriction of Nodal signaling during germ layer patterning.
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Registered trials
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.