ArticleNature2020
Tension heterogeneity directs form and fate to pattern the myocardial wall.
Article in Nature, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 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
75 citing papers in PubMed, 127 citations in OpenAlex.
- Article
- Notch-mediated lateral inhibition is shaped by morphological differences to reinforce bias toward signal-sending or -receiving roles.Current biology : CB · 2026Article
- Article
- A noncanonical role for Jagged1 in endothelial mechanotransduction.The FEBS journal · 2026Article
- Ex vivo imaging reveals neutrophil behaviors in the adult zebrafish heart.Journal of cell science · 2026Article
- The Notch1 intracellular domain orchestrates mechanotransduction of fluid shear stress.Life science alliance · 2026Article
- Regionalized regulation of actomyosin organization influences cardiomyocyte cell shape changes during chamber curvature formation.Nature communications · 2026Article
- Adgrg6/Gpr126 is required for compact wall integrity and establishing trabecular identity during cardiac trabeculation.Nature communications · 2026Article
- Nonmuscle α-Actinin-4 Couples Sarcomere Function to Cardiac Remodeling.Circulation research · 2026Article
- Coordination of cardiogenesis in vivo and in vitro.Nature reviews. Molecular cell biology · 2026Review
- Primordial cardiomyocytes orchestrate myocardial morphogenesis and vascularization but are dispensable for regeneration.bioRxiv : the preprint server for biology · 2025Article
- Interplay of ECM organization, ROCK signaling, and cell polarity drives mesothelium formation and lung growth.Nature communications · 2025Article
- New Genetic Loci Implicated in Cardiac Morphology and Function Using Three-Dimensional Population Phenotyping.Circulation. Genomic and precision medicine · 2025Article
- The gain and loss of plasticity during development and evolution.Trends in cell biology · 2025Review
- Mechanically activated snai1b coordinates the initiation of myocardial delamination for trabeculation.Nature communications · 2025Article
- A thermodynamic perspective on mammalian neural crest ingression.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Cardiac Development, Cellular Composition and Function: From Regulatory Mechanisms to Applications.Cells · 2025Review
- Epithelial tension controls intestinal cell extrusion.Science (New York, N.Y.) · 2025Article
- A role for Myosin in triggering and executing amnioserosa cell delaminations during dorsal closure.Scientific reports · 2025Article
- Gremlin1 repression-mediated mitochondrial network hyperfunction contributes to TCE-induced zebrafish cardiac defects.Cell communication and signaling : CCS · 2025Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
How diverse cell fates and complex forms emerge and feed back to each other to sculpt functional organs remains unclear. In the developing heart, the myocardium transitions from a simple epithelium to an intricate tissue that consists of distinct layers: the outer compact and inner trabecular layers. Defects in this process, which is known as cardiac trabeculation, cause cardiomyopathies and embryonic lethality, yet how tissue symmetry is broken to specify trabecular cardiomyocytes is unknown. Here we show that local tension heterogeneity drives organ-scale patterning and cell-fate decisions during cardiac trabeculation in zebrafish. Proliferation-induced cellular crowding at the tissue scale triggers tension heterogeneity among cardiomyocytes of the compact layer and drives those with higher contractility to delaminate and seed the trabecular layer. Experimentally, increasing crowding within the compact layer cardiomyocytes augments delamination, whereas decreasing it abrogates delamination. Using genetic mosaics in trabeculation-deficient zebrafish models-that is, in the absence of critical upstream signals such as Nrg-Erbb2 or blood flow-we find that inducing actomyosin contractility rescues cardiomyocyte delamination and is sufficient to drive cardiomyocyte fate specification, as assessed by Notch reporter expression in compact layer cardiomyocytes. Furthermore, Notch signalling perturbs the actomyosin machinery in cardiomyocytes to restrict excessive delamination, thereby preserving the architecture of the myocardial wall. Thus, tissue-scale forces converge on local cellular mechanics to generate complex forms and modulate cell-fate choices, and these multiscale regulatory interactions ensure robust self-organized organ 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.