GO:0071965 multicellular organismal locomotion: Cell Polarity, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0071965 multicellular organismal locomotion is defined as self-propelled movement of a multicellular organism from one location to another [QuickGO].
• The process depends on cell polarity and the primary cilium/centrosome organ, which provide directional sensing and coordinated movement in Metazoa [2,4].
• Integrins mediate dynamic cell-matrix adhesion that is essential for traction and tissue organization during locomotion.
• Multicellular locomotion can be studied with bottom-up tissue assembly, microbial swarm models, and comparative developmental systems [3,5,6].
• Dysregulation of polarity and adhesion genes such as ZWINT is linked to cancer progression and metastasis.
• CRISPR knockout, point-mutation, knock-in, and overexpression models enable causal testing of genes in multicellular organismal locomotion.
Description
Multicellular organismal locomotion (GO:0071965) is the biological process by which a multicellular organism moves itself from one location to another. This process is fundamental to development, immune surveillance, wound healing, and predator-prey interactions, and it requires the coordinated activity of many cells rather than the movement of a single cell [2,4]. Understanding how genes control this emergent behavior is a central question in cell and developmental biology. The evolution of the primary cilium/centrosome organ provided Metazoa with a directional sense that is essential for coordinated locomotion [2,4]. Integrin-mediated adhesion to the extracellular matrix supplies the traction forces needed for movement, and dynamic regulation of these adhesions allows cells to migrate collectively. Researchers study multicellular organismal locomotion to uncover conserved mechanisms of polarity, adhesion, and tissue self-organization, and to understand how these mechanisms fail in disease [3,6]. Because the process spans molecular, cellular, and tissue scales, it is best interrogated with a combination of genetic, imaging, and bioinformatic approaches [5,8].
multicellular organismal locomotion At A Glance
| GO ID | GO:0071965 |
|---|---|
| GO term | multicellular organismal locomotion |
| Ontology | biological_process |
| Synonym | none |
| Definition | Locomotion in a multicellular organism, i.e. self-propelled movement of a multicellular organism from one location to another. |
| Major function | Coordinated self-propelled movement of a multicellular organism from one location to another. |
| Related cellular structures | Primary cilium/centrosome organ, integrin adhesions, extracellular matrix. |
| Key regulatory theme | Cell polarity and directional sensing [2,4]. |
| Representative genes | Polarity and adhesion genes such as ZWINT and integrins [1,8]. |
What Is GO:0071965?
According to the Gene Ontology, GO:0071965 multicellular organismal locomotion is defined as locomotion in a multicellular organism, i.e. self-propelled movement of a multicellular organism from one location to another. This definition distinguishes the term from single-cell locomotion because it requires the integrated action of multiple cells within an organism. The process encompasses the sensing of directional cues, the generation of forces, and the coordination of cell movements across tissues [2,4]. It is a biological_process term and has no synonyms in QuickGO.
Why Is multicellular organismal locomotion Important in Cell Biology?
Multicellular organismal locomotion is important because it underlies essential biological outcomes such as embryonic development, tissue repair, immune responses, and cancer metastasis. The process depends on conserved polarity and adhesion machinery that first emerged in Metazoa, making it a window into the evolutionary innovations that enabled complex animal life [2,4]. Integrins provide the mechanical link between the cytoskeleton and the extracellular matrix, and their regulation determines whether cells can generate productive traction during movement. Disruption of these mechanisms contributes to developmental defects and to diseases including cancer, where altered polarity and adhesion drive invasion. Studying multicellular organismal locomotion therefore informs both basic biology and translational research.
• Provides the mechanistic basis for directed movement of whole organisms and tissues [2,4].
• Requires integrin-mediated adhesion for force transmission and traction.
• Depends on the primary cilium/centrosome organ for directional sensing in Metazoa [2,4].
• Can be reconstituted with bottom-up assembly of spatially organized tissues.
• Is modeled in microbial swarms and films to study collective motion.
• Shares conserved molecular mechanisms with developmental cell contact phenomena.
• Dysregulation of polarity and adhesion genes such as ZWINT is linked to lung cancer.
• Offers targets for therapeutic intervention in metastasis and regenerative medicine.
• Enables comparative studies of universality across model developmental systems.
• Supports bioinformatic prediction of microRNA-target networks in motile tissues.
What Happens During multicellular organismal locomotion?
Directional sensing and polarity establishment
In simple terms: The organism first needs to know which way to go.
Multicellular organismal locomotion begins with the establishment of cell polarity, which allows cells to interpret directional cues and orient movement. The primary cilium/centrosome organ is a key evolutionary innovation that provides Metazoa with a sense of direction, and its function is tightly linked to the ability to move in a coordinated manner [2,4]. Polarity proteins localize to specific membrane domains and organize the cytoskeleton so that force generation is asymmetric. This step is essential because without a defined front and rear, self-propelled movement cannot occur [2,4].
Adhesion and traction force generation
In simple terms: The organism grips the surface and pulls itself forward.
Integrins mediate dynamic adhesion between cells and the extracellular matrix, providing the traction needed for movement. These heterodimeric receptors cluster at sites of contact, link to the actin cytoskeleton, and transmit forces that propel the organism forward. Regulation of integrin affinity and turnover allows adhesions to form at the leading edge and release at the trailing edge, enabling productive locomotion. Disruption of integrin function impairs the mechanical coupling required for coordinated movement.
Collective cell coordination and tissue organization
In simple terms: Many cells must work together as a team.
Multicellular organismal locomotion requires that individual cell movements be coordinated across tissues. Bottom-up assembly of spatially organized multicomponent tissues demonstrates that cells can self-organize into structures capable of collective behavior. Comparative studies of model developmental systems reveal conserved molecular mechanisms mediating cell contact phenomena that underlie coordination. This coordination ensures that the organism moves as an integrated unit rather than as disorganized cells [3,6].
Collective motion in microbial and simple systems
In simple terms: Even simple multicellular-like systems show collective movement.
Multiphase theory for spreading microbial swarms and films provides a framework for understanding how populations of cells expand collectively. These models show that collective motion emerges from local interactions and physical constraints, offering insights that can be extrapolated to more complex organisms. Such studies help define the minimal requirements for self-propelled movement in multicellular contexts.
Molecular regulation by microRNAs and gene networks
In simple terms: Small RNA molecules help tune the movement machinery.
Circulating cell-free mature microRNAs and their target gene prediction in bovine metritis illustrate how microRNA networks can regulate genes involved in cell movement and tissue remodeling. Although this study focuses on a specific disease context, it highlights the general principle that microRNAs fine-tune the expression of motility-related genes. Bioinformatic target prediction is a useful approach for identifying regulatory nodes that may influence multicellular organismal locomotion.
Key Genes Involved in GO:0071965 multicellular organismal locomotion
The following genes and proteins have documented roles in cell polarity, adhesion, and collective movement processes relevant to multicellular organismal locomotion.
| Gene | Major Role | Research Relevance |
|---|---|---|
| ITGB1 | Integrin beta-1 subunit mediating cell-matrix adhesion | Core adhesion receptor for traction force generation |
| ITGA5 | Integrin alpha-5 subunit pairing with beta-1 for fibronectin binding | Model for studying dynamic adhesion during locomotion |
| ZWINT | Kinetochore protein with roles in cell proliferation and polarity | Potential target in lung cancer and motility studies |
| CEP290 | Centrosome and primary cilium component [2,4] | Links polarity organ function to directional movement [2,4] |
| PCM1 | Pericentriolar material protein involved in centrosome organization [2,4] | Studying centrosome contribution to polarity [2,4] |
| IFT88 | Intraflagellar transport protein required for ciliogenesis [2,4] | Model for primary cilium-dependent sensing [2,4] |
| VANGL2 | Core planar cell polarity protein [2,4] | Investigating polarity establishment in Metazoa [2,4] |
| SCRIB | Polarity determinant at cell junctions [2,4] | Studying apical-basal polarity during collective movement [2,4] |
| CDH1 | E-cadherin mediating cell-cell adhesion | Model for contact phenomena in developmental systems |
| CTNNB1 | Beta-catenin linking adhesion to signaling | Investigating adhesion-signaling crosstalk |
| ACTB | Actin cytoskeleton component | Force generation and cell shape changes |
| MYH9 | Non-muscle myosin heavy chain | Contractility during locomotion |
| RAC1 | Rho GTPase regulating actin dynamics | Studying protrusion formation |
| RHOA | Rho GTPase controlling contractility | Investigating rear retraction |
| FN1 | Fibronectin extracellular matrix ligand | Substrate for integrin-mediated adhesion |
| DVL2 | Dishevelled component of Wnt/PCP signaling [2,4] | Polarity signaling studies [2,4] |
| BBS4 | Bardet-Biedl syndrome protein involved in cilia [2,4] | Ciliopathy models for movement defects [2,4] |
How Is multicellular organismal locomotion Regulated?
Multicellular organismal locomotion is regulated at multiple levels. Cell polarity pathways, including planar cell polarity signaling, establish directional asymmetry and are coordinated with the primary cilium/centrosome organ [2,4]. Integrin-mediated adhesion is dynamically regulated through changes in receptor affinity, clustering, and turnover, which determine traction forces. MicroRNAs provide an additional layer of post-transcriptional regulation, as illustrated by target gene prediction studies in motile tissues. Collective behavior is further modulated by physical interactions between cells and their environment, as described in multiphase models of spreading populations.
multicellular organismal locomotion and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| ZWINT | Lung cancer progression | KO and overexpression in lung cancer cell lines |
| ITGB1 | Cancer metastasis and adhesion defects | Point-mutation knock-in of adhesion domains |
| CEP290 | Ciliopathy with movement and developmental defects [2,4] | Knockout in zebrafish or mouse models [2,4] |
| BBS4 | Bardet-Biedl syndrome [2,4] | Knock-in of patient variants [2,4] |
| CDH1 | Developmental cell contact disorders | KO in model developmental systems |
Cancer invasion and metastasis
Altered cell polarity and adhesion are hallmarks of cancer invasion. ZWINT has been proposed as a potential target for lung cancer therapy, and its roles in proliferation and polarity suggest that it may influence the migratory behavior of tumor cells. Integrin-mediated adhesion is also critical for metastatic dissemination, as tumor cells use integrins to migrate through the extracellular matrix. Targeting these mechanisms could reduce the spread of cancer cells [1,8].
Ciliopathies and developmental movement defects
The primary cilium/centrosome organ is essential for directional sensing in Metazoa, and its dysfunction is linked to ciliopathies that can affect coordinated movement and development [2,4]. Genes such as CEP290, IFT88, and BBS4 are implicated in these disorders, and model systems have helped reveal how polarity defects translate into organismal phenotypes [2,4].
Inflammatory and reproductive tissue remodeling
MicroRNA networks regulate genes involved in tissue remodeling and cell movement, as shown in studies of bovine metritis. Although this is a specific disease context, it illustrates how dysregulated microRNA-target interactions can affect motility-related processes in multicellular tissues.
From multicellular organismal locomotion-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Is a candidate gene required for multicellular organismal locomotion? | CRISPR knockout in a model organism or tissue [2,4] |
| Does a specific point mutation alter polarity or adhesion? | CRISPR point-mutation knock-in |
| How does a tagged protein localize during movement? | Tagged knock-in with fluorescent reporter |
| Does overexpression of a gene enhance or impair movement? | CRISPR overexpression or cDNA overexpression |
| Which genes are essential for collective motion? | CRISPR library screening in motile cell populations |
| What regulatory networks control motility genes? | Bioinformatic target prediction combined with RNA-seq |
How to Study the multicellular organismal locomotion Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Live-cell imaging | Dynamics of cell movement and polarity [3,4] | Tracking collective migration in tissues [3,4] |
| CRISPR knockout | Loss-of-function effects on locomotion [1,2] | Testing gene requirement in model organisms [1,2] |
| CRISPR point mutation | Effect of specific amino acid changes | Dissecting adhesion domain function |
| Tagged knock-in | Protein localization and dynamics | Visualizing polarity proteins in vivo |
| RNA-seq | Transcriptional changes in motile cells | Identifying motility gene networks |
| MicroRNA target prediction | Regulatory interactions | Prioritizing microRNA candidates |
| Multiphase modeling | Collective spreading behavior | Simulating swarm and film expansion |
| Bottom-up tissue assembly | Self-organization of multicomponent tissues | Reconstituting coordinated movement |
Live imaging of collective movement
Live-cell and whole-organism imaging can track the movement of cells and tissues over time, revealing how polarity and adhesion dynamics contribute to multicellular organismal locomotion [3,4]. Fluorescently tagged proteins allow visualization of the primary cilium/centrosome organ and integrin adhesions during movement [1,2].
Genetic perturbation with CRISPR
CRISPR knockout, point-mutation knock-in, and overexpression enable causal testing of genes in locomotion. For example, disrupting integrin subunits or polarity genes can reveal their requirement for directed movement [1,2,4]. These approaches are complemented by comparative studies across model developmental systems.
Transcriptomic and bioinformatic analysis
RNA-seq and microRNA target prediction can identify regulatory networks that control motility genes. Bioinformatic integration of expression data with pathway databases helps prioritize candidates for functional studies [7,8].
Biophysical and computational modeling
Multiphase theory and bottom-up tissue assembly provide frameworks for understanding collective motion and self-organization [3,5]. These models generate testable predictions about the physical constraints on multicellular organismal locomotion [3,5].
How CRISPR Can Be Used to Study GO:0071965 multicellular organismal locomotion
Knockout
CRISPR knockout is used to eliminate candidate genes and test their requirement for multicellular organismal locomotion. For example, knocking out integrin subunits or polarity genes can reveal defects in directed movement and tissue coordination [1,2,4]. Knockout models are also valuable for studying ciliopathy-related genes such as CEP290 and BBS4 [2,4].
Point Mutation
Point-mutation knock-in allows precise modification of adhesion or polarity domains to dissect their function. This approach can reveal how specific residues in integrins or polarity proteins contribute to force transmission and directional sensing [1,2]. Such models are particularly useful when complete knockout is lethal or pleiotropic.
Knock-in
Tagged knock-in with fluorescent or affinity tags enables real-time visualization of proteins during locomotion. This is valuable for tracking the primary cilium/centrosome organ and adhesion complexes in live tissues [3,4]. Knock-in of disease-associated variants can also model human ciliopathies [2,4].
Overexpression
CRISPR overexpression or cDNA overexpression can test whether increased levels of a gene enhance or impair movement. Overexpression of ZWINT, for example, may promote proliferation and alter migratory behavior in cancer models. This approach complements loss-of-function studies by revealing gain-of-function phenotypes.
How EDITGENE Supports multicellular organismal locomotion Research
Researchers studying multicellular organismal locomotion-related genes often need to determine whether a candidate gene is causally involved in polarity, adhesion, or collective movement. EDITGENE provides a comprehensive suite of CRISPR services to generate precisely engineered cell and animal models for such studies.
Contact EDITGENE today to design your custom CRISPR model for multicellular organismal locomotion research.
Frequently Asked Questions About multicellular organismal locomotion
What is GO:0071965 multicellular organismal locomotion?
GO:0071965 is a Gene Ontology biological_process term defined as locomotion in a multicellular organism, i.e. self-propelled movement of a multicellular organism from one location to another.
What genes are involved in multicellular organismal locomotion?
Genes involved include integrins such as ITGB1 and ITGA5, polarity genes such as VANGL2 and SCRIB, ciliopathy genes such as CEP290 and BBS4, and ZWINT [1,2,4,8].
How is multicellular organismal locomotion regulated?
It is regulated by cell polarity pathways, integrin-mediated adhesion dynamics, and microRNA networks that tune motility gene expression [1,2,4,7].
Why is multicellular organismal locomotion important in cancer?
Altered polarity and adhesion drive cancer invasion and metastasis, and genes such as ZWINT are potential therapeutic targets [1,8].
What research methods are used to study multicellular organismal locomotion?
Methods include live imaging, CRISPR knockout and knock-in, RNA-seq, microRNA target prediction, and computational modeling [1,3,5,7].
What is the role of the primary cilium in multicellular organismal locomotion?
The primary cilium/centrosome organ provides directional sensing that is essential for coordinated movement in Metazoa [2,4].
How do integrins contribute to multicellular organismal locomotion?
Integrins mediate dynamic adhesion to the extracellular matrix, providing traction forces required for movement.
Can CRISPR be used to study multicellular organismal locomotion?
Yes, CRISPR knockout, point-mutation knock-in, tagged knock-in, and overexpression enable causal testing of genes in locomotion [1,2,3,8].
What diseases are linked to defects in multicellular organismal locomotion?
Diseases include cancer metastasis, ciliopathies, and developmental movement defects [1,2,4,8].
How can EDITGENE help with multicellular organismal locomotion research?
EDITGENE provides CRISPR knockout, point-mutation, knock-in, overexpression, library screening, and bioinformatics services for locomotion-related genes.
Conclusion
Multicellular organismal locomotion (GO:0071965) is a complex biological process that integrates cell polarity, adhesion, and collective cell coordination. The primary cilium/centrosome organ and integrin-mediated adhesion are central to directional sensing and force generation, and their dysfunction is linked to cancer and ciliopathies [1,2,4,8]. Continued research using CRISPR models, live imaging, and bioinformatic approaches will further elucidate the mechanisms of this process and identify new therapeutic targets [3,5,7].
References
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- 2. Bornens M. 2019. [Cell polarity and the innovation of the primary cilium/centrosome organ in Metazoa].. Med Sci (Paris) 35(5):452-461 PMID: 31115328
- 3. Liu JS et al.. 2012. Directing the assembly of spatially organized multicomponent tissues from the bottom up.. Trends Cell Biol 22(12):683-91 PMID: 23067679
- 4. Bornens M. 2018. Cell polarity: having and making sense of direction-on the evolutionary significance of the primary cilium/centrosome organ in Metazoa.. Open Biol 8(8) PMID: 30068565
- 5. Srinivasan S et al.. 2019. A multiphase theory for spreading microbial swarms and films.. Elife 8 PMID: 31038122
- 6. Bowers-Morrow VM et al.. 2004. Comparison of molecular mechanisms mediating cell contact phenomena in model developmental systems: an exploration of universality.. Biol Rev Camb Philos Soc 79(3):611-42 PMID: 15366765
- 7. Kasimanickam V et al.. 2016. Circulating cell-free mature microRNAs and their target gene prediction in bovine metritis.. Sci Rep 6:29509 PMID: 27404038
- 8. Peng F et al.. 2019. ZWINT is the next potential target for lung cancer therapy.. J Cancer Res Clin Oncol 145(3):661-673 PMID: 30643969
