GO:0035787 cell migration involved in kidney development: Mechanism, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0035787 describes the orderly movement of cells that contributes to kidney development from formation to the mature organ.
• Cell migration in kidney development depends on adhesion molecules such as EpCAM and integrins that mediate cell-cell and cell-matrix interactions.
• Disruption of migratory programs is linked to renal disease, including lupus nephritis and diabetic kidney disease.
• Metabolic and epigenetic signals, such as fumarate accumulation, can induce epithelial-to-mesenchymal transition and alter migratory behavior.
• Key genes studied in this context include CXCL10, CXCR3, EpCAM, integrins, and metabolic regulators such as SLC28A1.
• CRISPR knockout, knock-in, and overexpression models enable causal testing of candidate genes in kidney cell migration.
Description
Cell migration involved in kidney development (GO:0035787) is a biological process defined as the orderly movement of a cell from one site to another that contributes to the progression of the kidney over time, from its formation to the mature organ. This process is fundamental to nephrogenesis, where precise spatial and temporal cell movements ensure correct patterning of the renal parenchyma and vasculature. Researchers study this term to understand how migratory cues are integrated during development and how their dysregulation contributes to congenital anomalies and acquired kidney diseases. The ontology term captures a developmental context rather than a generic motility program, emphasizing the kidney as the anatomical system in which migration occurs. Because cell migration intersects with adhesion, signaling, and metabolic pathways, it serves as a nexus for interrogating both normal organogenesis and disease mechanisms.
cell migration involved in kidney development At A Glance
| GO ID | GO:0035787 |
|---|---|
| GO term | cell migration involved in kidney development |
| Ontology | biological_process |
| Synonym | none |
| Major function | Orderly cell movement that contributes to kidney formation and maturation |
| Related processes | Cell adhesion, epithelial-to-mesenchymal transition, angiogenesis |
| Key molecules | EpCAM, integrins, CXCL10-CXCR3 axis, metabolic regulators |
| Disease relevance | Lupus nephritis, diabetic kidney disease, renal cell carcinoma |
What Is GO:0035787?
In our own words, GO:0035787 refers to the directed, coordinated movement of individual cells that is required for the kidney to form and mature properly. It encompasses the migration of progenitor and differentiated cell types as they relocate to build nephrons, the collecting system, and the renal vasculature. This term is distinct from general cell motility because its outcome is explicitly tied to kidney development, from the earliest embryonic stages through to the mature organ.
Why Is cell migration involved in kidney development Important in Cell Biology?
Understanding cell migration involved in kidney development is critical because it bridges basic developmental biology and clinical nephrology. Migratory events during kidney formation establish the architectural blueprint of the organ, and when these processes go awry, they can lead to malformations or predispose to disease. Moreover, reactivation of developmental migratory programs in adulthood contributes to pathological conditions such as glomerular endothelial cell migration in diabetic kidney disease and immune cell recruitment in lupus nephritis. Studying this term therefore offers insights into both congenital and acquired kidney disorders, and it provides a framework for identifying therapeutic targets that modulate cell movement.
• Essential for nephrogenesis and proper patterning of the renal parenchyma.
• Involved in recruitment of mesenchymal stem cells in lupus nephritis.
• Contributes to glomerular endothelial cell migration in diabetic kidney disease.
• Regulated by adhesion molecules such as EpCAM and integrins.
• Linked to epithelial-to-mesenchymal transition via metabolic signals like fumarate.
• Provides a context for studying CXCL10-CXCR3 chemokine axis in kidney injury.
• Relevant to clear cell renal cell carcinoma progression through metabolic transporters.
• Offers targets for CRISPR-based functional genomics in kidney models.
• Helps explain how developmental programs are reactivated in adult disease.
• Guides design of cell-based therapies requiring directed migration.
What Happens During cell migration involved in kidney development?
Initiation and directional sensing
In simple terms: Cells first receive signals that tell them where to go.
Migratory cells in the developing kidney respond to chemotactic cues and adhesion signals that establish polarity and directionality. Adhesion molecules such as EpCAM and integrins mediate initial cell-matrix interactions that are required for movement. The CXCL10-CXCR3 axis can recruit mesenchymal stem cells to sites of renal remodeling, illustrating how chemokine gradients direct migration in kidney contexts.
Adhesion dynamics and cytoskeletal rearrangement
In simple terms: Cells grip and release surfaces while reshaping their internal skeleton to move.
Integrins and other adhesion receptors form dynamic contacts with the extracellular matrix, allowing cells to generate traction forces. EpCAM participates in morphogenetic processes by modulating cell adhesion and signaling. These adhesion events are coupled to reorganization of the actin cytoskeleton, which propels the cell forward during kidney development.
Epithelial-to-mesenchymal transition and plasticity
In simple terms: Some cells change from stationary to migratory by altering their identity.
Epithelial-to-mesenchymal transition (EMT) is a key mechanism that enables cells to acquire migratory capacity. Fumarate accumulation can act as an epigenetic modifier that elicits EMT, linking metabolic state to migratory behavior. This plasticity is important for cells that must relocate during kidney formation and for pathological migration in disease.
Integration with angiogenesis and vascular patterning
In simple terms: Migrating cells help build the kidney's blood vessel network.
Cell migration involved in kidney development is closely coordinated with angiogenesis. In diabetic kidney disease, inhibiting glomerular endothelial cell migration delays progression, highlighting the interplay between migratory and angiogenic programs. Proper vascular patterning depends on timely movement of endothelial and mural cells during development.
Key Genes Involved in GO:0035787 cell migration involved in kidney development
The following genes and proteins have been experimentally implicated in cell migration involved in kidney development or related renal migratory processes.
| Gene | Major Role | Research Relevance |
|---|---|---|
| CXCL10 | Chemokine that recruits CXCR3+ cells | Studied in lupus nephritis for mesenchymal stem cell recruitment |
| CXCR3 | Receptor for CXCL10 | Mediates chemotaxis in renal remodeling |
| EpCAM | Adhesion molecule in morphogenesis | Regulates cell adhesion during kidney development |
| SLC28A1 | Nucleoside transporter affecting metabolism | Linked to clear cell renal cell carcinoma progression |
| Integrins (e.g., ITGB1) | Cell-matrix adhesion receptors | Essential for kidney cell migration and disease |
| IL4I1 | Enzyme secreted by mesenchymal stem cells | Modulates immune and renal remodeling |
| Fumarate (FH-related) | Metabolic intermediate and epigenetic modifier | Induces EMT and migratory phenotype |
| Cyp17a2 | Steroidogenic enzyme | Studied in testicular development; model for gonadal migration |
| VEGFA | Angiogenic factor | Influences endothelial migration in kidney |
| CDH1 (E-cadherin) | Epithelial adhesion | Loss promotes EMT and migration |
| VIM | Mesenchymal marker | Upregulated during EMT in migratory cells |
| ACTA2 | Smooth muscle actin | Marker of mesenchymal transition |
| FN1 | Extracellular matrix protein | Supports integrin-mediated migration |
| COL4A1 | Basement membrane collagen | Integrin ligand in kidney |
| LAMA5 | Laminin subunit | Cell adhesion in renal development |
| CDH2 (N-cadherin) | Mesenchymal adhesion | Associated with migratory phenotype |
| MMP2 | Matrix metalloproteinase | Facilitates matrix remodeling during migration |
| MMP9 | Matrix metalloproteinase | Degrades matrix to permit cell movement |
How Is cell migration involved in kidney development Regulated?
Cell migration involved in kidney development is regulated by a combination of chemokine gradients, adhesion receptor signaling, and metabolic cues. The CXCL10-CXCR3 axis recruits mesenchymal stem cells and modulates renal remodeling. Integrin signaling provides dynamic control of adhesion strength and cytoskeletal organization. EpCAM influences morphogenetic movements through its role in cell adhesion. Metabolic signals such as fumarate can epigenetically reprogram cells to undergo EMT, thereby promoting migratory capacity. In disease contexts, inhibition of glomerular endothelial cell migration can delay progression, indicating that migratory programs are actively regulated and targetable.
cell migration involved in kidney development and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| CXCL10/CXCR3 | Lupus nephritis | Knockout mice or human cell lines with CXCR3 KO |
| SLC28A1 | Clear cell renal cell carcinoma | Overexpression and knockout in ccRCC cell lines |
| Integrins | Kidney fibrosis and inflammation | Conditional integrin knockout in mouse kidney |
| EpCAM | Kidney malformations | EpCAM knockout or knockdown in zebrafish |
| FH (fumarate hydratase) | Hereditary leiomyomatosis and renal cell cancer | FH-deficient cell models with fumarate accumulation |
Lupus nephritis and immune cell recruitment
In lupus nephritis, the CXCL10-CXCR3 axis recruits mesenchymal stem cells to the kidney, and subsequent IL4I1 secretion contributes to renal remodeling. This highlights how migratory processes originally important in development can be reactivated in autoimmune kidney injury.
Diabetic kidney disease and endothelial migration
Glomerular endothelial cell migration contributes to abnormal angiogenesis in diabetic kidney disease. Inhibiting this migration with hirudin delays disease progression, suggesting that migratory pathways are viable therapeutic targets.
Clear cell renal cell carcinoma and metabolic transporters
SLC28A1, a nucleoside transporter, inhibits clear cell renal cell carcinoma progression by affecting arachidonic acid metabolism. This links metabolic regulation to migratory and invasive behavior in kidney cancer.
Epigenetic regulation and EMT in kidney pathology
Fumarate accumulation acts as an epigenetic modifier that elicits epithelial-to-mesenchymal transition, a process that confers migratory properties on cells. This mechanism connects metabolic dysregulation to fibrotic and malignant kidney diseases.
From cell migration involved in kidney development-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does CXCR3 mediate mesenchymal stem cell migration in lupus nephritis? | CXCR3 knockout mice or CRISPR KO in human MSCs |
| Does SLC28A1 affect ccRCC migration and metabolism? | SLC28A1 overexpression and knockout in ccRCC lines |
| Is EpCAM required for kidney morphogenesis? | EpCAM knockout zebrafish or mouse |
| Do integrins regulate kidney cell migration? | Conditional integrin knock-in/knockout mice |
| Does fumarate induce EMT and migration? | FH knockout or fumarate-treated kidney cells |
| Can hirudin inhibit glomerular endothelial migration? | Diabetic kidney disease mouse models treated with hirudin |
How to Study the cell migration involved in kidney development Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Live-cell imaging | Directional movement and speed | Kidney organoid migration assays |
| RNA-seq | Transcriptional changes | Comparing migratory vs stationary cells |
| Proteomics | Protein expression and modifications | Adhesion complex dynamics |
| CRISPR knockout | Loss-of-function effects | Testing candidate genes in migration |
| CRISPR knock-in | Tagged or mutant protein function | Tracking endogenous proteins |
| Overexpression | Gain-of-function effects | Assessing sufficiency of a gene |
| Chemotaxis assays | Directed migration response | Testing CXCL10-CXCR3 axis |
| Wound healing assay | Collective cell migration | Evaluating endothelial migration |
Live imaging of migrating cells
Time-lapse microscopy of fluorescently labeled cells in organotypic cultures or zebrafish embryos allows direct visualization of cell migration during kidney development.
Transcriptomic profiling of migratory cells
RNA-seq of sorted migratory populations can identify genes and pathways enriched during kidney development and disease.
Proteomic and phosphoproteomic analysis
Mass spectrometry-based proteomics reveals changes in adhesion and cytoskeletal proteins during migration.
Functional perturbation with CRISPR
CRISPR knockout, knock-in, and overexpression enable causal testing of candidate genes in migration assays.
How CRISPR Can Be Used to Study GO:0035787 cell migration involved in kidney development
Knockout
CRISPR knockout of genes such as CXCR3 or SLC28A1 can reveal their requirement for cell migration in kidney development and disease models.
Point Mutation
Introducing point mutations in adhesion molecules like EpCAM or integrins allows structure-function analysis of migratory signaling.
Knock-in
Knock-in of fluorescent tags or disease-associated variants into endogenous loci enables real-time tracking of migratory cells and functional studies.
Overexpression
Overexpression of candidates such as SLC28A1 or chemokines can test sufficiency for promoting or inhibiting migration in kidney cells.
How EDITGENE Supports cell migration involved in kidney development Research
Researchers studying cell migration involved in kidney development-related genes often need to determine whether a candidate gene is causally involved in migratory behavior or simply correlated with it. EDITGENE provides the tools to move from observation to mechanism.
Contact EDITGENE today to design your custom CRISPR model for cell migration involved in kidney development research.
Frequently Asked Questions About cell migration involved in kidney development
What is GO:0035787?
GO:0035787 is the Gene Ontology term for cell migration involved in kidney development, defined as the orderly movement of a cell that contributes to kidney progression from formation to the mature organ.
What genes are involved in cell migration involved in kidney development?
Key genes include CXCL10, CXCR3, EpCAM, integrins, SLC28A1, and metabolic regulators such as fumarate hydratase.
How is cell migration involved in kidney development studied?
Researchers use live imaging, RNA-seq, proteomics, and CRISPR perturbation in cell and animal models.
Why is cell migration important in kidney development?
It ensures correct patterning of nephrons and vasculature; disruption can lead to malformations and disease.
What diseases are linked to cell migration involved in kidney development?
Lupus nephritis, diabetic kidney disease, and clear cell renal cell carcinoma have been linked to migratory processes.
What is the role of EpCAM in kidney development?
EpCAM is an adhesion molecule that participates in morphogenetic movements during kidney development.
How do integrins regulate kidney cell migration?
Integrins mediate cell-matrix adhesion and signaling that are required for migratory behavior in kidney cells.
Can CRISPR be used to study kidney cell migration?
Yes, CRISPR knockout, knock-in, and overexpression models enable causal testing of genes in migration assays.
What is the CXCL10-CXCR3 axis in kidney disease?
It is a chemokine-receptor axis that recruits mesenchymal stem cells to the kidney in lupus nephritis.
How does fumarate affect cell migration?
Fumarate acts as an epigenetic modifier that induces epithelial-to-mesenchymal transition, promoting migratory capacity.
Conclusion
GO:0035787 cell migration involved in kidney development is a fundamental biological process that integrates adhesion, signaling, and metabolism to build and maintain the kidney. Its dysregulation contributes to a spectrum of renal diseases, from autoimmune nephritis to cancer. By leveraging CRISPR-based models and multi-omics approaches, researchers can dissect the causal roles of specific genes and identify new therapeutic targets.
References
- 1. Zhang Q et al.. 2024. Renal remodeling by CXCL10-CXCR3 axis-recruited mesenchymal stem cells and subsequent IL4I1 secretion in lupus nephritis.. Signal Transduct Target Ther 9(1):325 PMID: 39557841
- 2. Trzpis M et al.. 2008. EpCAM in morphogenesis.. Front Biosci 13:5050-5 PMID: 18508569
- 3. Li J et al.. 2026. SLC28A1 inhibits clear cell renal cell carcinoma progression by affecting arachidonic acid metabolism: A novel nucleoside transporter-based targeted therapy strategy.. Cancer Lett 649:218481 PMID: 41946263
- 4. Zhang J et al.. 2024. Hirudin delays the progression of diabetic kidney disease by inhibiting glomerular endothelial cell migration and abnormal angiogenesis.. Biomed Pharmacother 179:117300 PMID: 39178812
- 5. Perantoni AO. 1999. Cell adhesion molecules in the kidney: from embryo to adult.. Exp Nephrol 7(2):80-102 PMID: 10213863
- 6. Pozzi A et al.. 2013. Integrins in kidney disease.. J Am Soc Nephrol 24(7):1034-9 PMID: 23641054
- 7. Yang L et al.. 2022. Cyp17a2 is involved in testicular development and fertility in male Nile tilapia, Oreochromis niloticus.. Front Endocrinol (Lausanne) 13:1074921 PMID: 36523590
- 8. Sciacovelli M et al.. 2016. Fumarate is an epigenetic modifier that elicits epithelial-to-mesenchymal transition.. Nature 537(7621):544-547 PMID: 27580029
