Evidence map›Paper›PMID 40948237›Full record

ArticleDevelopment (Cambridge, England)2025

Synergistic and independent roles for Nodal and FGF in zebrafish cardiac progenitor cell migration and asymmetric heart morphogenesis.

Vanessa Gonzalez, Meagan G Grant, Makoto Suzuki, Briana Christophers, Jessica Rowland Williams, Rebecca D Burdine

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Development (Cambridge, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Vanessa GonzalezDepartment of Molecular Biology, Princeton University, Princeton, NJ 08544, USA.ORCID 0000-0001-5524-4465
Meagan G GrantDepartment of Molecular Biology, Princeton University, Princeton, NJ 08544, USA.
Makoto SuzukiDepartment of Molecular Biology, Princeton University, Princeton, NJ 08544, USA.ORCID 0000-0002-5494-6593
Briana ChristophersDepartment of Molecular Biology, Princeton University, Princeton, NJ 08544, USA.ORCID 0000-0001-5248-069X
Jessica Rowland WilliamsDepartment of Molecular Biology, Princeton University, Princeton, NJ 08544, USA.
Rebecca D BurdineDepartment of Molecular Biology, Princeton University, Princeton, NJ 08544, USA.ORCID 0000-0001-6620-5015

Funding

PREDOCTORAL TRAINING PROGRAM IN GENETICST32GM007388 · NIGMS · PRINCETON UNIVERSITY · PI CRISTEA, ILEANA M. · 1985 to 2022
$27.4M
Connecting Polycystin Signaling to Asymmetric Nodal ExpressionR01HD048584 · NICHD · PRINCETON UNIVERSITY · PI BURDINE, REBECCA D. · 2007 to 2016
$3.5M
American Heart Association 24PRE1198653Directorate for Biological Sciences IOS-1147123JanssenJanssen Scholars of Oncology FellowshipNational Institute of Child Health and Human Development R01HD048584National Institutes of Natural SciencesNational Science Foundation IOS-1147123National Science Foundation Graduate Research Fellowship ProgramNew Jersey Commission on Cancer Research COCR24PRG007NICHD NIH HHS R01 HD048584NIGMS NIH HHS T32 GM007388NIGMS NIH HHS T32GM007388Princeton UniversityState of New Jersey Commission on Cancer Research COCR24PRG007
6 · The paper itself

Abstract

Asymmetric development of the vertebrate heart is driven by a complex sequence of morphogenetic cell movements, coordinated through precise interpretation of signaling cues by the heart primordia. Here, we show that Nodal signaling functions synergistically with FGF to stimulate the migration of cardiac progenitor cells (CPCs) during cardiac jogging - the first morphological asymmetry observed in zebrafish heart development. While Nodal directs the asymmetric migration of CPCs, we find FGF signaling to be dispensable for this asymmetry, suggesting that FGF plays a permissive rather than instructive role. We further demonstrate that Nodal signaling induces asymmetries in actin cytoskeletal dynamics that correlate with the directional migration of CPCs, whereas FGF does not influence this actin asymmetry. In addition to influencing jogging, FGF and Nodal synergize to ensure proper heart looping. We also provide evidence that FGF contributes to heart looping by promoting the differentiation of the second heart field. Together, these findings offer insight into how the spatiotemporal dynamics of signaling pathways regulate the cellular behaviors driving organ morphogenesis.

Indexed as

Cell MovementFibroblast Growth FactorsHeartMorphogenesisNodal ProteinStem CellsZebrafishZebrafish ProteinsActin CytoskeletonAnimalsCell DifferentiationGene Expression Regulation, DevelopmentalMyocardiumOrganogenesisSignal TransductionFibroblast Growth FactorsNodal ProteinZebrafish ProteinsCardiac joggingCardiac loopingCongenital heart defectsLeft-right asymmetryZebrafish

Identifiers

PMID40948237
PMCPMC12539208

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Registered trials

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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.