GO:0051673 disruption of plasma membrane integrity in another organism: Cytolysis Mechanism, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0051673 describes the disruption of another organism's plasma membrane, leading to damage or temporary subversion of the membrane.
• Pore-forming toxins (PFTs) are the best-characterized effectors that execute this process, assembling into membrane-inserted pores that compromise barrier function.
• Membrane repair machinery, including TRIM72 and mitochondria-derived MOTS-c, counteracts membrane disruption and is essential for cell survival.
• Disruption of plasma membrane integrity is central to bacterial pathogenesis, immune defense, and viral entry, making it a high-value target for therapeutic intervention.
• Experimental dissection of this process relies on CRISPR knockout, point-mutation, knock-in, and overexpression models combined with imaging and cytotoxicity assays [6,7].
• Dysregulated membrane integrity contributes to diseases ranging from colitis and thoracic aortic dissection to neurodegeneration and cancer [2,4,5].
Description
The Gene Ontology term GO:0051673, disruption of plasma membrane integrity in another organism, captures a fundamental biological process in which one organism damages or temporarily subverts the plasma membrane of another. This process is a shared strategy across bacterial pathogens, viruses, and immune effectors, and it often determines whether an infection establishes, whether a target cell survives, or whether an immune response eliminates a threat. Because the plasma membrane is the primary barrier between a cell and its environment, its disruption triggers rapid ionic imbalance, loss of ATP, and activation of repair or death programs. Understanding the molecular players that execute and counteract this process is therefore central to infection biology, immunology, and cell stress research [6,7]. Mechanistically, disruption of plasma membrane integrity in another organism is frequently mediated by pore-forming toxins (PFTs) that bind target membranes, oligomerize, and insert into the lipid bilayer to create conductive pores. These pores dissipate electrochemical gradients and allow uncontrolled flux of ions, small metabolites, and proteins, which can lead to osmotic lysis or programmed cell death. Host cells respond by deploying membrane repair systems, including the TRIM72-dependent repair pathway and mitochondria-encoded peptides such as MOTS-c that facilitate repair factor translocation. The balance between disruption and repair determines cellular outcome and has direct implications for tissue homeostasis and disease. For researchers, GO:0051673 provides a precise ontological handle for annotating genes and pathways involved in cytolysis, host-pathogen interaction, and membrane repair. It enables systematic comparison of effectors across organisms and supports functional genomics screens that identify host factors required for susceptibility or resistance to membrane-disrupting agents [6,7]. As CRISPR-based models become routine, the ability to knock out, mutate, or tag components of this process accelerates mechanistic discovery and therapeutic target validation [6,7].
disruption of plasma membrane integrity in another organism At A Glance
| GO ID | GO:0051673 |
|---|---|
| GO term | disruption of plasma membrane integrity in another organism |
| Ontology | biological_process |
| Synonym | cytolysis, by membrane disruption, in other organism; disruption by organism of host cell membrane; disruption by virus of host cell membrane; disruption of membrane integrity in another organism; membrane disruption in another organism; membrane disruption in other organism; perturbation of plasma membrane integrity in another organism |
| Major function | Damage or temporary subversion of another organism's plasma membrane, often through pore formation or permeabilization |
| Cellular context | Plasma membrane of the target cell; frequently involves secreted or surface-associated effectors from the attacking organism |
| Representative effectors | Pore-forming toxins (PFTs) such as cholesterol-dependent cytolysins and other membrane-inserting proteins |
| Counteracting systems | Membrane repair machinery including TRIM72 and MOTS-c-dependent pathways |
| Disease relevance | Bacterial infection, colitis, thoracic aortic dissection, neurodegeneration, and cancer [2,4,5] |
What Is GO:0051673?
GO:0051673, disruption of plasma membrane integrity in another organism, is defined as the disruption of the cell membrane of another organism, leading to damage or temporary subversion of the membrane. In practice, this term covers processes by which a bacterium, virus, or other organism compromises the plasma membrane barrier of a target cell, including pore formation, membrane permeabilization, and cytolysis. It is a biological process annotation that can be applied to effectors such as pore-forming toxins and to host factors that mediate or counteract membrane damage [6,7].
Why Is disruption of plasma membrane integrity in another organism Important in Cell Biology?
Disruption of plasma membrane integrity in another organism is a decisive event in host-pathogen interactions because it can directly determine cell fate, tissue damage, and immune activation. Pore-forming toxins that mediate this process are among the most widespread virulence factors in bacterial pathogens, and their activity is often sufficient to cause cytolysis or to trigger inflammatory signaling. At the same time, host membrane repair pathways such as the TRIM72-MOTS-c axis are required to survive sublethal membrane damage, and their failure sensitizes cells to injury. Studying GO:0051673 therefore bridges microbiology, immunology, and cell biology, and it offers a rational basis for developing anti-virulence drugs, vaccine adjuvants, and cytoprotective strategies [6,7].
• Pore-forming toxins that execute GO:0051673 are key virulence factors in bacterial infection and immunity.
• Membrane disruption triggers ionic imbalance, ATP loss, and osmotic lysis, directly influencing cell survival.
• Host membrane repair pathways, including TRIM72 and MOTS-c, counteract disruption and are essential for tissue resilience.
• The process is implicated in intestinal barrier dysfunction and colitis through tight junction and membrane integrity crosstalk.
• Disruption of endothelial focal adhesions and membrane integrity contributes to thoracic aortic dissection.
• Extracellular phosphate and inflammation can modulate cytotoxicity and membrane damage in disease contexts.
• Desmosomal and junctional proteins that maintain membrane integrity are linked to human diseases when compromised.
• CRISPR screens targeting membrane-disrupting effectors and repair factors can identify host susceptibility genes [6,7].
• The term provides a standardized annotation for comparative genomics of virulence and immune effector mechanisms.
• Therapeutic strategies that block pore formation or enhance membrane repair are emerging from this research area [6,7].
What Happens During disruption of plasma membrane integrity in another organism?
Recognition and binding of the target membrane
In simple terms: The attacking organism first sticks to the target cell membrane.
The process begins when an effector molecule produced by one organism recognizes and binds to the plasma membrane of another organism. This binding is often mediated by specific lipid or protein receptors and determines target cell specificity. For pore-forming toxins, receptor engagement concentrates the effector on the membrane surface and primes it for subsequent assembly steps.
Oligomerization and pore assembly
In simple terms: Many toxin molecules gather together to form a ring-like pore.
After binding, many pore-forming toxins undergo oligomerization to form a prepore complex on the membrane surface. This assembly step is frequently dependent on cholesterol or other membrane components and can involve conformational changes that expose hydrophobic regions. The prepore then transitions to a membrane-inserted pore, creating a conductive channel that breaches the lipid bilayer.
Membrane insertion and permeabilization
In simple terms: The pore punches through the membrane, letting ions and small molecules leak out.
Membrane insertion of the pore-forming complex disrupts plasma membrane integrity, allowing uncontrolled flux of ions, ATP, and small metabolites. This permeabilization dissipates electrochemical gradients and can lead to osmotic swelling and cytolysis. The extent of damage depends on pore number, size, and the availability of repair mechanisms [6,7].
Host membrane repair response
In simple terms: The cell tries to patch the holes in its membrane.
Target cells respond to membrane disruption by activating repair pathways that reseal the plasma membrane. The mitochondria-encoded peptide MOTS-c participates in plasma membrane repair by facilitating the translocation of TRIM72 to the membrane. This repair response can rescue cells from sublethal damage and is critical for maintaining tissue integrity during infection.
Downstream outcomes: survival, lysis, or signaling
In simple terms: Depending on the damage, the cell may recover, die, or send alarm signals.
If repair succeeds, the cell can survive and may activate inflammatory or stress signaling [6,7]. If disruption overwhelms repair capacity, the cell undergoes lysis or programmed death, releasing damage-associated signals that shape immune responses. These outcomes are central to the pathogenesis of infections and to the efficacy of immune effector mechanisms.
Key Genes Involved in GO:0051673 disruption of plasma membrane integrity in another organism
The following genes and proteins represent major effectors, regulators, and repair factors associated with GO:0051673, based on published literature.
| Gene | Major Role | Research Relevance |
|---|---|---|
| TRIM72 | Facilitates plasma membrane repair by translocating to damaged membrane sites | Knockout and knock-in models to study repair efficiency and cytoprotection |
| MOTS-c | Mitochondria-encoded peptide that promotes TRIM72 translocation for membrane repair | Overexpression and knockout models to dissect mitochondrial regulation of repair |
| ZO-1 | Tight junction protein whose degradation compromises epithelial barrier integrity | Autophagy-mediated degradation models in colitis research |
| PEAK1 | Maintains tight junctions in intestinal epithelial cells by inhibiting autophagy-mediated ZO-1 degradation | Knockout models to study barrier dysfunction and colitis susceptibility |
| Calpain-2 | Mediates endothelial focal adhesion disruption in thoracic aortic dissection | Point-mutation and knockout models for vascular integrity studies |
| Desmosomal cadherins | Maintain desmosome-mediated cell adhesion and membrane integrity | Disease modeling for desmosomal disorders |
| Pore-forming toxins (PFTs) | Execute membrane disruption by forming pores in target membranes | Structural and functional studies of virulence mechanisms |
| Cholesterol-dependent cytolysins | Representative PFT family that oligomerizes on cholesterol-rich membranes | Membrane binding and pore assembly assays |
| Extracellular phosphate sensors | Modulate cytotoxicity and inflammation in response to phosphate load | In vitro models of phosphate-induced membrane damage |
| Inflammatory cytokines | Amplify tissue damage and modulate membrane integrity under stress | Co-culture and cytokine stimulation models |
| Autophagy machinery | Regulates degradation of junctional proteins and membrane components | Knockout and pharmacological inhibition studies |
| Focal adhesion components | Anchor cells to matrix and are disrupted during endothelial injury | Live imaging and adhesion assays |
| Mitochondrial quality control factors | Support energy supply for membrane repair | Isolation and functional assays of mitochondria |
| Biomimetic outer membrane nanoparticles | Model bacterial outer membrane interactions with host cells | Delivery and repair studies in spinal cord injury |
| TRIM72-associated E3 ligase machinery | Regulates membrane repair protein turnover | Proteomic and interaction studies |
| Calpain family proteases | Cleave focal adhesion and membrane-associated proteins | Inhibitor and knockout studies |
| Tight junction scaffolds | Maintain epithelial barrier and limit paracellular flux | Barrier function assays in colitis models |
How Is disruption of plasma membrane integrity in another organism Regulated?
Regulation of disruption of plasma membrane integrity in another organism operates at multiple levels. Effector production and secretion are controlled by bacterial quorum sensing and host-derived signals, while pore assembly can be modulated by membrane lipid composition and cholesterol availability. On the host side, membrane repair is regulated by calcium-dependent pathways and by the TRIM72-MOTS-c axis, which couples mitochondrial status to repair capacity. Inflammatory mediators and extracellular phosphate can sensitize or protect cells from membrane damage, linking metabolic and immune signals to the outcome of disruption. Tight junction and desmosomal proteins further modulate tissue-level susceptibility to membrane perturbation [2,8].
disruption of plasma membrane integrity in another organism and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| TRIM72 | Membrane repair deficiency and cytoprotection | Knockout and knock-in cell lines with membrane damage assays |
| PEAK1 | Colitis and intestinal barrier dysfunction | Intestinal epithelial knockout models and colitis induction |
| Calpain-2 | Thoracic aortic dissection and endothelial injury | Point-mutation and knockout endothelial cells |
| Desmosomal cadherins | Desmosomal disorders and tissue fragility | Knock-in disease mutations in keratinocytes |
| Pore-forming toxins | Bacterial infection and cytolysis | Toxin challenge assays in target cell lines |
Bacterial infection and pore-forming toxin-mediated disease
Many bacterial pathogens rely on pore-forming toxins to disrupt host cell membranes, causing tissue damage and promoting infection. This process is a major driver of cytolysis and inflammation in diseases such as pneumonia, sepsis, and enteric infections. Understanding how PFTs execute GO:0051673 informs anti-virulence strategies and vaccine development.
Intestinal barrier dysfunction and colitis
Disruption of plasma membrane and junctional integrity in intestinal epithelial cells contributes to barrier dysfunction and colitis. PEAK1 maintains tight junctions by inhibiting autophagy-mediated ZO-1 degradation, and its loss sensitizes cells to barrier disruption. This links membrane integrity pathways to inflammatory bowel disease pathogenesis.
Vascular injury and thoracic aortic dissection
Calpain-2-mediated endothelial focal adhesion disruption compromises vascular integrity and contributes to thoracic aortic dissection. Membrane and adhesion disruption in endothelial cells is a key event in this life-threatening condition. Models of calpain-2 inhibition or knockout are used to study protective mechanisms.
Neurodegeneration and tissue repair
Membrane disruption and impaired repair are increasingly recognized in neurodegenerative and injury contexts [7,3]. MOTS-c-dependent membrane repair supports cell survival under stress, and biomimetic outer membrane nanoparticles have been explored for spinal cord injury repair [7,3]. These findings highlight the therapeutic potential of targeting membrane integrity pathways [7,3].
From disruption of plasma membrane integrity in another organism-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does loss of TRIM72 impair membrane repair? | TRIM72 knockout cell line |
| Does a point mutation in a pore-forming toxin abolish pore assembly? | Point-mutation knock-in of the toxin gene |
| Can tagged TRIM72 be used to track repair dynamics? | Knock-in of fluorescent tag at the TRIM72 locus |
| Does overexpression of MOTS-c enhance membrane repair? | MOTS-c overexpression cell line |
| Does PEAK1 loss sensitize cells to barrier disruption? | PEAK1 knockout intestinal epithelial cells |
| Does calpain-2 inhibition protect endothelial integrity? | Calpain-2 knockout or inhibitor-treated endothelial cells |
How to Study the disruption of plasma membrane integrity in another organism Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Live-cell imaging | Real-time membrane integrity and repair dynamics | Pore formation and resealing kinetics |
| LDH release assay | Cytotoxicity and membrane damage | Toxin challenge experiments |
| Propidium iodide uptake | Membrane permeabilization | Screening for membrane-disrupting effectors |
| Co-immunoprecipitation | Protein-protein interactions in repair complexes | Identifying TRIM72 interactors |
| CRISPR knockout screen | Host genes affecting susceptibility | Functional genomics of membrane disruption |
| Mitochondrial isolation | Mitochondrial function and MOTS-c production | Studying mitochondrial contributions to repair |
| Nanoparticle delivery assays | Biomimetic membrane interactions | Spinal cord injury repair models |
| Barrier function assays | Epithelial tight junction integrity | Colitis and permeability studies |
Live-cell imaging of membrane integrity
Live-cell imaging with membrane-impermeant dyes and fluorescently tagged repair proteins allows real-time visualization of pore formation and resealing. This approach is essential for quantifying the kinetics of disruption and repair in response to pore-forming toxins [6,7].
Cytotoxicity and permeability assays
Lactate dehydrogenase release, propidium iodide uptake, and ATP leakage assays measure the extent of plasma membrane disruption. These assays are widely used to compare wild-type and mutant effectors or host factors.
Proteomics and interaction studies
Affinity purification and mass spectrometry can identify host proteins that interact with pore-forming toxins or repair machinery. Such studies reveal the molecular network underlying membrane disruption and repair.
CRISPR-based functional genomics
Genome-wide CRISPR knockout screens can identify host genes required for susceptibility or resistance to membrane-disrupting agents [6,7]. These screens provide unbiased discovery of new regulators of GO:0051673 [6,7].
How CRISPR Can Be Used to Study GO:0051673 disruption of plasma membrane integrity in another organism
Knockout
CRISPR knockout of host genes such as TRIM72 or PEAK1 enables researchers to test their requirement for membrane repair or barrier maintenance [7,2]. Knockout cell lines challenged with pore-forming toxins reveal whether a gene is protective or sensitizing [6,7].
Point Mutation
Point mutations can be introduced into effector genes to dissect domains required for membrane binding, oligomerization, or pore insertion. In host genes, point mutations can mimic disease-associated variants that alter repair capacity.
Knock-in
Knock-in of fluorescent or epitope tags at endogenous loci allows tracking of repair proteins such as TRIM72 in real time. Knock-in of disease-relevant mutations provides physiologically relevant models of membrane integrity disorders.
Overexpression
Overexpression of MOTS-c or other repair factors can enhance membrane repair and protect cells from disruption. Overexpression of pore-forming toxins or their subunits is used to study gain-of-function effects on membrane integrity.
How EDITGENE Supports disruption of plasma membrane integrity in another organism Research
Researchers studying disruption of plasma membrane integrity in another organism-related genes often need to determine whether a candidate gene is causally involved in membrane damage, repair, or host susceptibility. EDITGENE provides end-to-end CRISPR services that enable precise genetic models for mechanistic and translational studies of GO:0051673.
Contact EDITGENE today to design your custom CRISPR model for disruption of plasma membrane integrity in another organism research.
Frequently Asked Questions About disruption of plasma membrane integrity in another organism
What is GO:0051673?
GO:0051673 is the Gene Ontology term for disruption of plasma membrane integrity in another organism, defined as the disruption of the cell membrane of another organism, leading to damage or temporary subversion of the membrane.
What genes are involved in disruption of plasma membrane integrity in another organism?
Key genes include TRIM72 and MOTS-c in membrane repair, PEAK1 and ZO-1 in barrier integrity, and calpain-2 in endothelial adhesion disruption, alongside pore-forming toxin genes from pathogens [7,2,4,6].
How do pore-forming toxins disrupt membranes?
Pore-forming toxins bind target membranes, oligomerize into prepores, and insert into the lipid bilayer to form conductive pores that permeabilize the cell.
What is the role of TRIM72 in membrane repair?
TRIM72 translocates to damaged membrane sites to facilitate repair, and this process is promoted by the mitochondria-encoded peptide MOTS-c.
Which diseases are linked to plasma membrane disruption?
Bacterial infections, colitis, thoracic aortic dissection, and neurodegenerative or injury conditions are linked to membrane disruption and impaired repair [6,2,4,7].
How can CRISPR be used to study GO:0051673?
CRISPR knockout, point mutation, knock-in, and overexpression models allow researchers to test the causal role of specific genes in membrane disruption and repair [6,7].
What methods measure membrane integrity disruption?
Live-cell imaging, LDH release, propidium iodide uptake, and ATP leakage assays are commonly used to quantify membrane disruption [6,7].
Is disruption of plasma membrane integrity in another organism a biological process?
Yes, GO:0051673 is annotated as a biological_process in the Gene Ontology.
What is the difference between cytolysis and membrane disruption?
Cytolysis is a synonym for this term and refers to the lytic outcome of membrane disruption, whereas membrane disruption can also be sublethal and reversible through repair [6,7].
How does PEAK1 protect intestinal barrier integrity?
PEAK1 maintains tight junctions by inhibiting autophagy-mediated ZO-1 degradation, thereby resisting colitis-associated barrier disruption.
Conclusion
GO:0051673, disruption of plasma membrane integrity in another organism, is a central biological process that governs the outcome of host-pathogen interactions and tissue injury. Its molecular basis involves pore-forming effectors that breach the membrane and host repair pathways such as the TRIM72-MOTS-c axis that restore integrity [6,7]. Dysregulation of this process is linked to infectious, inflammatory, and vascular diseases, making it a compelling target for therapeutic development [6,2,4]. CRISPR-based models and functional genomics screens provide powerful tools to dissect the underlying mechanisms and to identify new intervention points [6,7].
References
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- 2. Zhang Z et al.. 2025. PEAK1 maintains tight junctions in intestinal epithelial cells and resists colitis by inhibiting autophagy-mediated ZO-1 degradation.. Nat Commun 16(1):6777 PMID: 40707483
- 3. Li P et al.. 2025. Spatiotemporal Targeted Delivery of Biomimetic Bacterial Outer Membrane Nanoparticles for Enhanced Spinal Cord Injury Repair.. Adv Mater 37(30):e2502795 PMID: 40391641
- 4. Teng X et al.. 2025. Calpain-2-Mediated Endothelial Focal Adhesion Disruption in Thoracic Aortic Dissection.. Adv Sci (Weinh) 12(25):e2501112 PMID: 40171827
- 5. Michigami T et al.. 2022. Extracellular Phosphate, Inflammation and Cytotoxicity.. Adv Exp Med Biol 1362:15-25 PMID: 35288869
- 6. Verma P et al.. 2021. Pore-forming toxins in infection and immunity.. Biochem Soc Trans 49(1):455-465 PMID: 33492383
- 7. Jia H et al.. 2024. Mitochondria-encoded peptide MOTS-c participates in plasma membrane repair by facilitating the translocation of TRIM72 to membrane.. Theranostics 14(13):5001-5021 PMID: 39267782
- 8. Najor NA. 2018. Desmosomes in Human Disease.. Annu Rev Pathol 13:51-70 PMID: 29414250
