ArticlePLoS genetics2013
Integration of nodal and BMP signals in the heart requires FoxH1 to create left-right differences in cell migration rates that direct cardiac asymmetry.
Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
35 citing papers in PubMed, 67 citations in OpenAlex.
- MicroRNA expression, target genes, and signaling pathways in infants with a ventricular septal defect.Molecular and cellular biochemistry · 2018Trial
- Global Evaluation of Congenital Heart Disease-Associated Non-Coding Variants.Research square · 2026Article
- Synergistic and independent roles for Nodal and FGF in zebrafish cardiac progenitor cell migration and asymmetric heart morphogenesis.Development (Cambridge, England) · 2025Article
- Zebrafish as a Versatile Model for Cardiovascular Research: Peering into the Heart of the Matter.Cells · 2025Review
- Differentiation of Pluripotent Stem Cells for Disease Modeling: Learning from Heart Development.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Next-generation plasmids for transgenesis in zebrafish and beyond.Development (Cambridge, England) · 2023Article
- Nodal signaling regulates asymmetric cellular behaviors, driving clockwise rotation of the heart tube in zebrafish.Communications biology · 2022Article
- Sequential action of JNK genes establishes the embryonic left-right axis.Development (Cambridge, England) · 2022Article
- Understanding laterality disorders and the left-right organizer: Insights from zebrafish.Frontiers in cell and developmental biology · 2022Review
- Of form and function: Early cardiac morphogenesis across classical and emerging model systems.Seminars in cell & developmental biology · 2021Review
- Getting to the Heart of Left-Right Asymmetry: Contributions from the Zebrafish Model.Journal of cardiovascular development and disease · 2021Review
- From Stripes to a Beating Heart: Early Cardiac Development in Zebrafish.Journal of cardiovascular development and disease · 2021Review
- Cell chirality in cardiovascular development and disease.APL bioengineering · 2020Review
- Swimming toward solutions: Using fish and frogs as models for understanding RASopathies.Birth defects research · 2020Review
- Making and breaking symmetry in development, growth and disease.Development (Cambridge, England) · 2019Review
- Intrinsic cellular chirality regulates left-right symmetry breaking during cardiac looping.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- The Role of Abnormal Placentation in Congenital Heart Disease; Cause, Correlate, or Consequence?Frontiers in physiology · 2018Article
- Establishing the Embryonic Axes: Prime Time for Teratogenic Insults.Journal of cardiovascular development and disease · 2017Review
- Left-Right Patterning: Breaking Symmetry to Asymmetric Morphogenesis.Trends in genetics : TIG · 2017Review
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Failure to properly establish the left-right (L/R) axis is a major cause of congenital heart defects in humans, but how L/R patterning of the embryo leads to asymmetric cardiac morphogenesis is still unclear. We find that asymmetric Nodal signaling on the left and Bmp signaling act in parallel to establish zebrafish cardiac laterality by modulating cell migration velocities across the L/R axis. Moreover, we demonstrate that Nodal plays the crucial role in generating asymmetry in the heart and that Bmp signaling via Bmp4 is dispensable in the presence of asymmetric Nodal signaling. In addition, we identify a previously unappreciated role for the Nodal-transcription factor FoxH1 in mediating cell responsiveness to Bmp, further linking the control of these two pathways in the heart. The interplay between these TGFβ pathways is complex, with Nodal signaling potentially acting to limit the response to Bmp pathway activation and the dosage of Bmp signals being critical to limit migration rates. These findings have implications for understanding the complex genetic interactions that lead to congenital heart disease in humans.
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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.