GO:0060973 cell migration involved in heart development: Developmental Cell Migration, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0060973 describes the orderly movement of cells that contributes to heart formation and maturation, from the initial heart field to the mature organ.
• Cardiac neural crest cells, epicardial cells, and cardiomyocytes are among the key migratory cell populations in heart development.
• Slit-Robo, FGF, and Nrg1 signaling pathways are established regulators of cell migration during cardiogenesis.
• Disrupted cell migration in heart development is linked to congenital heart defects and impaired cardiac repair after injury.
• CRISPR knockout, point mutation, knock-in, and overexpression models enable causal testing of migration-related genes in cardiac development.
• Single-cell multi-omics and lineage tracing are increasingly used to resolve migratory cell states in heart development and disease.
Description
Cell migration involved in heart development (GO:0060973) is a biological process defined as the orderly movement of a cell from one site to another that contributes to the progression of the heart over time, from its initial formation to the mature organ. This process is fundamental to cardiogenesis because the heart is assembled from multiple progenitor populations that must migrate, coalesce, and differentiate in a spatially and temporally coordinated manner. Without precise migratory cues, cardiac structures such as the outflow tract, ventricles, and coronary vasculature fail to form correctly.
cell migration involved in heart development At A Glance
| GO ID | GO:0060973 |
|---|---|
| GO term | cell migration involved in heart development |
| Ontology | biological_process |
| Synonym | None |
| Major function | Coordinated cell movement that contributes to heart formation and maturation |
| Related cell types | Cardiac neural crest cells, epicardial cells, cardiomyocytes, endothelial cells |
| Key signaling pathways | Slit-Robo, FGF, Nrg1, EZH2-dependent epigenetic regulation |
| Disease relevance | Congenital heart defects, impaired cardiac repair, myocarditis-associated migration |
What Is GO:0060973?
In simple terms, GO:0060973 covers all the directed cell movements that help build and mature the heart. It includes the migration of cardiac neural crest cells into the outflow tract, the movement of epicardial cells over the heart surface, and the migration of cardiomyocytes during ventricular development. The term is a biological process and is part of the broader ontology of heart development and cell migration.
Why Is cell migration involved in heart development Important in Cell Biology?
Understanding GO:0060973 is critical because defects in cardiac cell migration underlie some of the most common congenital heart defects and contribute to poor cardiac repair after injury. Researchers studying heart development, regenerative medicine, and cardiovascular disease need to know which genes control these migratory events and how their dysfunction leads to pathology.
• Cardiac neural crest cell migration is essential for outflow tract septation and aortic arch patterning.
• Epicardial cell migration supports coronary vessel formation and myocardial growth.
• Slit-Robo signaling guides multiple migratory cell populations in the developing heart.
• FGF signaling controls vascular development and metabolic states that influence migration.
• Nrg1 regulates cardiomyocyte migration and cell cycle during ventricular development.
• Disrupted migration contributes to congenital heart defects and impaired post-injury repair.
• Single-cell multi-omics can identify migratory immune cell subsets in cardiac inflammation.
• CRISPR-based models allow causal testing of migration genes in cardiac development.
What Happens During cell migration involved in heart development?
Specification and delamination of migratory cardiac progenitors
In simple terms: Cells first receive signals that tell them to become migratory and leave their original location.
Cardiac neural crest cells are specified at the dorsal neural tube and undergo an epithelial-to-mesenchymal transition to delaminate and migrate toward the heart. This step depends on precise transcriptional and signaling inputs that prime cells for directed movement.
Directed migration toward the heart field
In simple terms: Migratory cells follow chemical trails to reach the developing heart.
Slit-Robo signaling provides repulsive and attractive cues that guide cardiac neural crest and other progenitors to their correct destinations. FGF signaling also contributes to vascular and progenitor cell migration during heart development.
Epicardial cell migration over the heart surface
In simple terms: A sheet of cells spreads over the heart to form its outer layer and blood vessels.
Epicardial cells migrate from the proepicardium over the myocardium, a process controlled by epigenetic regulators such as EZH2. This migration is required for coronary vessel development and myocardial compaction.
Cardiomyocyte migration during ventricular development
In simple terms: Heart muscle cells move and rearrange to shape the ventricles.
Nrg1 regulates cardiomyocyte migration and cell cycle progression during ventricular development, influencing trabeculation and myocardial architecture. Disruption of this migration leads to ventricular defects.
Integration with vascular and immune cell migration
In simple terms: Other cell types also migrate into the heart to support its growth and respond to injury.
Angiogenesis after myocardial infarction involves endothelial cell migration that shares molecular cues with developmental migration. In acute myocarditis, specialized cytotoxic and migratory CD8+ effector T cells infiltrate the heart, highlighting migration as a shared theme in development and disease.
Key Genes Involved in GO:0060973 cell migration involved in heart development
The following genes and proteins have established roles in cell migration involved in heart development, based on published literature.
| Gene | Major Role | Research Relevance |
|---|---|---|
| SLIT2 | Ligand for Robo receptors guiding cardiac cell migration | Slit-Robo signaling in heart development |
| ROBO1 | Receptor mediating repulsive cues for migrating cardiac cells | Cardiac neural crest and outflow tract patterning |
| ROBO2 | Receptor involved in guidance of migratory cardiac progenitors | Heart development and congenital defects |
| EZH2 | Epigenetic regulator of epicardial cell migration | Epicardial migration and coronary development |
| NRG1 | Growth factor regulating cardiomyocyte migration and cell cycle | Ventricular development and trabeculation |
| FGF10 | Fibroblast growth factor controlling heart development and repair | FGF signaling in cardiogenesis |
| FGFR1 | Receptor for FGF ligands affecting vascular migration | Vascular development and metabolism |
| FGFR2 | Receptor mediating FGF-dependent migration cues | Heart development and homeostasis |
| VEGFA | Angiogenic factor promoting endothelial cell migration | Angiogenesis after myocardial infarction |
| CDH5 | Endothelial adhesion molecule in migrating vascular cells | Vascular development and repair |
| PECAM1 | Endothelial marker in migrating angiogenic cells | Post-infarction angiogenesis |
| CD8A | Marker of cytotoxic migratory T cells | Acute myocarditis immune migration |
| IFNG | Cytokine influencing migratory immune cell behavior | Myocarditis and cardiac inflammation |
| GATA4 | Transcription factor in cardiac development | Heart development and congenital defects |
| TBX1 | Transcription factor in cardiac neural crest and outflow tract | Cardiac neural crest migration |
| PAX3 | Neural crest specification and migration | Cardiac neural crest development |
| SOX10 | Neural crest migration and differentiation | Cardiac neural crest contribution to heart |
How Is cell migration involved in heart development Regulated?
Cell migration involved in heart development is regulated by multiple signaling and epigenetic mechanisms. Slit-Robo signaling provides guidance cues that direct migratory cardiac cells to their targets. FGF signaling, including FGF10 and its receptors, controls vascular development and metabolic states that influence cell migration. EZH2-dependent epigenetic regulation is required for epicardial cell migration. Nrg1 signaling regulates cardiomyocyte migration and cell cycle during ventricular development. In disease contexts, angiogenic and immune cell migration are regulated by factors such as VEGFA and inflammatory cytokines.
cell migration involved in heart development and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| SLIT2/ROBO1 | Congenital heart defects, outflow tract malformations | Knockout mouse, zebrafish |
| EZH2 | Epicardial migration defects, coronary anomalies | Conditional knockout mouse |
| NRG1 | Ventricular development defects, cardiomyopathy | Knockout and overexpression models |
| FGF10 | Heart development and repair defects | Knockout mouse, cell models |
| VEGFA | Impaired angiogenesis after myocardial infarction | Overexpression and knockout models |
Congenital heart defects
Disrupted migration of cardiac neural crest cells and epicardial cells leads to congenital heart defects, including outflow tract malformations and coronary anomalies. Slit-Robo and FGF signaling defects are associated with abnormal heart development.
Myocardial infarction and impaired repair
After acute myocardial infarction, angiogenesis requires endothelial cell migration to restore blood supply. Defects in migratory signaling impair cardiac repair and contribute to heart failure.
Acute myocarditis
In acute myocarditis, specialized cytotoxic and migratory CD8+ effector T cells infiltrate the myocardium, causing inflammation and damage. Understanding their migration may inform therapeutic strategies.
Cardiomyopathy and ventricular dysfunction
Altered cardiomyocyte migration during ventricular development, as seen with Nrg1 dysregulation, can lead to ventricular defects and cardiomyopathy.
From cell migration involved in heart development-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Is a gene required for cardiac neural crest migration? | CRISPR knockout in mouse or zebrafish |
| Does a point mutation in a migration gene cause congenital heart defects? | CRISPR point mutation knock-in |
| How does a tagged migration protein localize in live cells? | CRISPR knock-in of fluorescent tag |
| Does overexpression of a growth factor enhance cardiac repair? | CRISPR overexpression in cardiomyocytes or endothelial cells |
| Which genes regulate epicardial cell migration? | CRISPR library screening in epicardial cell cultures |
| What are the transcriptomic states of migratory cardiac cells? | Single-cell RNA-seq with lineage tracing |
How to Study the cell migration involved in heart development Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Lineage tracing | Origin and fate of migratory cells | Cardiac neural crest and epicardial migration |
| Live imaging | Real-time cell movement | Embryonic heart development |
| Single-cell RNA-seq | Transcriptomic states of migratory cells | Heart development and myocarditis |
| CRISPR knockout screening | Genes required for migration | Epicardial and cardiomyocyte migration |
| Phosphoproteomics | Signaling pathway activation | FGF and Slit-Robo signaling |
| Co-immunoprecipitation | Protein-protein interactions | Receptor-ligand complexes in migration |
| Immunofluorescence | Protein localization in migrating cells | Cardiac tissue sections |
| Bioinformatics pathway analysis | Enriched migration gene sets | Multi-omics data interpretation |
Lineage tracing and live imaging
Lineage tracing using genetic reporters allows visualization of migratory cardiac cell populations in vivo. Live imaging in zebrafish and mouse embryos captures dynamic migration events.
Single-cell multi-omics
Single-cell RNA-seq and multi-omics identify migratory cell states and regulatory networks in heart development and disease. This approach can resolve heterogeneity among cardiac neural crest, epicardial, and immune cells.
CRISPR screening and functional genomics
CRISPR knockout and activation screens in cardiac cell models can identify genes required for migration. These screens are complemented by bioinformatics analysis of migration-related gene signatures.
Protein interaction and signaling assays
Co-immunoprecipitation, proximity labeling, and phosphoproteomics can map signaling pathways such as Slit-Robo and FGF that control migration. These methods reveal how mutations affect protein function.
How CRISPR Can Be Used to Study GO:0060973 cell migration involved in heart development
Knockout
CRISPR knockout of genes such as EZH2 or NRG1 in cardiac cell models can test their requirement for cell migration during heart development. Knockout models reveal loss-of-function phenotypes and validate candidate genes from screens.
Point Mutation
CRISPR point mutation knock-in can model human variants in migration-related genes, such as those in SLIT2 or ROBO1, to assess their impact on cardiac cell movement. This approach links specific alleles to congenital heart defect risk.
Knock-in
Knock-in of fluorescent or epitope tags into endogenous migration genes allows real-time tracking of protein localization and dynamics in cardiac cells. Tagged knock-in models are valuable for imaging migratory events.
Overexpression
CRISPR-mediated overexpression of pro-migratory factors such as VEGFA or FGF10 can enhance endothelial or progenitor cell migration in models of cardiac repair. Overexpression studies help identify sufficiency of a gene for migration.
How EDITGENE Supports cell migration involved in heart development Research
Researchers studying cell migration involved in heart development-related genes often need to determine whether a candidate gene is causally involved in migration, and which variants alter its function. EDITGENE provides CRISPR-based cell models and screening services to accelerate this discovery.
Contact EDITGENE today to design your custom CRISPR model for cell migration involved in heart development research.
Frequently Asked Questions About cell migration involved in heart development
What is cell migration involved in heart development?
It is the orderly movement of cells that contributes to heart formation and maturation, defined as GO:0060973.
What genes are involved in cell migration involved in heart development?
Key genes include SLIT2, ROBO1, EZH2, NRG1, FGF10, and VEGFA, among others.
Why is cell migration important for heart development?
It ensures that cardiac neural crest cells, epicardial cells, and cardiomyocytes reach correct locations for proper heart structure and function.
What diseases are linked to defects in cardiac cell migration?
Congenital heart defects, impaired cardiac repair after myocardial infarction, and myocarditis are associated with migration defects.
How do Slit-Robo signals regulate heart development?
Slit-Robo signaling provides guidance cues that direct migratory cardiac cells to their targets during cardiogenesis.
What is the role of EZH2 in heart development?
EZH2 controls epicardial cell migration, which is essential for coronary vessel development.
How does Nrg1 affect cardiomyocyte migration?
Nrg1 regulates cardiomyocyte migration and cell cycle during ventricular development.
What research methods are used to study cardiac cell migration?
Lineage tracing, live imaging, single-cell RNA-seq, and CRISPR screens are commonly used.
Can CRISPR be used to study cell migration in heart development?
Yes, CRISPR knockout, point mutation, knock-in, and overexpression models enable causal testing of migration genes.
What cell types migrate during heart development?
Cardiac neural crest cells, epicardial cells, cardiomyocytes, endothelial cells, and immune cells can migrate during heart development and disease.
Conclusion
GO:0060973 cell migration involved in heart development is a central biological process that coordinates the movement of multiple cell populations to build and mature the heart. Its dysregulation contributes to congenital heart defects and impaired cardiac repair, making it a key area for cardiovascular research. Advances in CRISPR modeling and single-cell technologies continue to reveal the genes and mechanisms controlling this process.
References
- 1. Wu X et al.. 2021. Angiogenesis after acute myocardial infarction.. Cardiovasc Res 117(5):1257-1273 PMID: 33063086
- 2. Tong Z et al.. 2025. Single-Cell Multi-Omics Identifies Specialized Cytotoxic and Migratory CD8(+) Effector T Cells in Acute Myocarditis.. Circulation 152(14):1003-1022 PMID: 40762079
- 3. Zhao J et al.. 2018. Slit-Robo signalling in heart development.. Cardiovasc Res 114(6):794-804 PMID: 29538649
- 4. Yamagishi H. 2021. Cardiac Neural Crest.. Cold Spring Harb Perspect Biol 13(1) PMID: 32071091
- 5. Jiang H et al.. 2023. EZH2 controls epicardial cell migration during heart development.. Life Sci Alliance 6(6) PMID: 37037595
- 6. Yu P et al.. 2017. FGF-dependent metabolic control of vascular development.. Nature 545(7653):224-228 PMID: 28467822
- 7. Grego-Bessa J et al.. 2023. Nrg1 Regulates Cardiomyocyte Migration and Cell Cycle in Ventricular Development.. Circ Res 133(11):927-943 PMID: 37846569
- 8. Hubert F et al.. 2018. FGF10 Signaling in Heart Development, Homeostasis, Disease and Repair.. Front Genet 9:599 PMID: 30546382
