GO:0035821 modulation of process of another organism: Host-Pathogen Interaction Mechanisms, Genes, Functions and Research Methods

Research-grade guide for scientists and biopharma professionals

Key Takeaways

GO:0035821 describes any process by which one organism changes a biological process in another organism, including modification of host morphology, physiology, or immune signaling.
The term is deliberately broad and covers bacterial secretion of effector proteins, viral manipulation of host metabolism, and parasite-induced tissue remodeling.
Experimentally, modulation is detected by comparing host transcriptomes, proteomes, and metabolite profiles in the presence versus absence of the modulating organism.
Key effectors include secreted proteases, kinases, and pore-forming toxins that alter extracellular matrix turnover, ion homeostasis, and inflammatory signaling.
Dysregulated modulation underlies chronic infection, sepsis, fibrosis, and aging-related tissue dysfunction, making it a target for host-directed therapies.
CRISPR knockout, knock-in, and overexpression models in human cell lines enable causal testing of candidate host genes required for microbial modulation.

Description

GO:0035821, modulation of process of another organism, is a biological process ontology term defined as a process in which an organism effects a change in a biological process in another organism. Unlike terms that describe a single molecular activity, GO:0035821 captures the inter-organismal outcome: the modulating organism alters the physiology, morphology, or behavior of a second organism. This makes the term central to host-microbe interaction biology, where bacteria, viruses, fungi, and parasites actively reprogram host cells to promote their own survival and dissemination. The QuickGO synonyms, including modification of morphology or physiology of other organism and regulation of physiological process of other organism, emphasize that the target of modulation can be structural, metabolic, or signaling-related. For researchers, GO:0035821 provides a standardized annotation framework for experiments that measure cross-species perturbation. Studies of extracellular matrix remodeling show that microbial and parasitic factors can directly alter matrix assembly and turnover, changing tissue architecture in the host. Metabolomic investigations further demonstrate that infection reshapes host small-molecule profiles, providing readouts of physiological modulation. Because the term is agnostic to the specific mechanism, it accommodates secreted effectors, surface adhesins, and small-molecule signals that collectively determine disease outcomes. Understanding GO:0035821 is therefore essential for interpreting infection, inflammation, and tissue-repair data. It links mechanistic cell biology to organism-level phenotypes such as sodium imbalance in sepsis, fibrosis progression, and age-related functional decline. The sections below summarize the definition, core mechanisms, key genes, disease relevance, and CRISPR-based methods used to study this process.

modulation of process of another organism At A Glance

GO ID GO:0035821
GO term modulation of process of another organism
Ontology biological_process
Synonym modification of morphology or physiology of other organism; modulation of process of other organism; regulation of morphology of other organism; regulation of morphology or physiology of other organism; regulation of physiological process of other organism; regulation of physiology of other organism
Major function Cross-organism perturbation of host or partner physiology, morphology, or signaling
Taxonomic scope Broad; applies to bacteria, viruses, fungi, parasites, and their hosts
Typical effectors Secreted proteins, proteases, kinases, toxins, and small molecules
Experimental readouts Transcriptomics, proteomics, metabolomics, and imaging of host tissue

What Is GO:0035821?

In plain terms, GO:0035821 describes any situation where organism A changes how organism B works. The official QuickGO definition states: A process in which an organism effects a change in a biological process in another organism. This includes changes to the other organism's morphology, physiology, or regulatory pathways, and is often used to annotate host-pathogen interactions, symbiosis, and parasitism.

Why Is modulation of process of another organism Important in Cell Biology?

GO:0035821 matters because it formalizes how one organism can actively reprogram another, a phenomenon that determines the outcome of infection, symbiosis, and chronic inflammatory disease. Without a standardized term, researchers studying bacterial effectors, viral proteins, and parasite-derived factors would lack a common annotation language for cross-species perturbation. The term also connects mechanistic findings to clinically relevant phenotypes such as sepsis-associated ion imbalance, fibrosis, and aging-related tissue dysfunction.
Provides a unified ontology annotation for host-pathogen and symbiont-host interactions.
Enables comparative analysis of bacterial, viral, fungal, and parasitic effectors that alter host physiology.
Links microbial modulation to extracellular matrix remodeling and tissue architecture changes.
Supports metabolomic and proteomic studies of infection-induced physiological shifts.
Explains sepsis-related disturbances in sodium and water homeostasis.
Connects chronic modulation to fibrosis through mechanosensitive pathways such as Piezo1.
Provides a framework for studying aging as cumulative physiological modulation.
Guides anti-inflammatory and host-directed therapeutic strategies, including natural compounds.
Enables CRISPR-based causal testing of host genes required for microbial modulation.
Facilitates cross-species data integration in systems biology and bioinformatics pipelines.

What Happens During modulation of process of another organism?

Recognition and Attachment
In simple terms: The modulating organism first finds and sticks to the other organism or its cells.
Modulation begins with recognition of host or partner surfaces. Microbial adhesins, viral receptor-binding proteins, and parasite surface ligands mediate attachment and determine tissue tropism. This step is often accompanied by local changes in extracellular matrix composition that facilitate stable contact. In chemosensory and neural contexts, neuromodulatory signals can also alter host sensory processing, illustrating that recognition is not limited to pathogens.
Delivery of Modulatory Effectors
In simple terms: The organism injects or secretes molecules that change how the other organism behaves.
Once attached, bacteria, viruses, and parasites deliver effector molecules into host cells or the extracellular space. These effectors include proteases, kinases, phosphatases, and pore-forming toxins that modify host signaling and metabolism. Secreted proteases can degrade or remodel extracellular matrix components, while kinases can phosphorylate host proteins to alter immune signaling. The collective action of these effectors constitutes the molecular basis of GO:0035821.
Host Physiological and Metabolic Reprogramming
In simple terms: The other organism's metabolism and physiology are rewired.
Effector delivery leads to measurable changes in host metabolism, ion balance, and gene expression. Metabolomic studies reveal that infection alters small-molecule profiles, reflecting shifts in energy metabolism and biosynthetic pathways. Sodium homeostasis is particularly sensitive to microbial modulation, and disturbances in sodium balance are observed in sepsis. Aquaporins, which regulate water transport, are also modulated during sepsis, linking effector activity to fluid homeostasis.
Tissue Remodeling and Morphological Change
In simple terms: The structure of the other organism's tissues is physically changed.
Sustained modulation often results in tissue remodeling. Extracellular matrix assembly and turnover are actively regulated by microbial and host factors, and dysregulation contributes to fibrosis. Mechanosensitive channels such as Piezo1 translate mechanical changes into cellular responses that promote fibrotic remodeling. These morphological outcomes are a hallmark of GO:0035821 and can be visualized by imaging and histology.
Resolution or Chronic Persistence
In simple terms: The interaction either resolves or becomes long-lasting.
The outcome of modulation depends on host immunity and microbial persistence strategies. Acute modulation may resolve with immune clearance, whereas chronic modulation contributes to persistent infection, inflammation, and age-related tissue decline. Anti-inflammatory interventions, including bromelain, have been studied for their ability to dampen chronic inflammatory modulation. Understanding resolution versus persistence is critical for therapeutic targeting.

Key Genes Involved in GO:0035821 modulation of process of another organism

The following genes and proteins represent major functional categories involved in GO:0035821, including host receptors, effectors, matrix components, and signaling mediators.
GeneMajor RoleResearch Relevance
MMP2Matrix metalloproteinase that degrades extracellular matrixMatrix remodeling during infection and fibrosis
MMP9Matrix metalloproteinase involved in tissue remodelingHost tissue degradation in chronic inflammation
COL1A1Type I collagen, major extracellular matrix componentMatrix assembly and fibrosis readout
FN1Fibronectin, adhesive extracellular matrix proteinCell-matrix adhesion during microbial attachment
PIEZO1Mechanosensitive ion channelFibrosis and mechanotransduction
AQP1Aquaporin water channelWater homeostasis in sepsis
AQP5Aquaporin water channelEpithelial fluid transport during infection
SCNN1AEpithelial sodium channel subunitSodium homeostasis in sepsis
ATP1A1Na+/K+-ATPase subunitIon balance and physiological modulation
IL6Pro-inflammatory cytokineInflammatory modulation and chronic disease
TNFPro-inflammatory cytokineHost response to microbial effectors
NFKB1Transcription factor controlling inflammationSignaling node modulated by effectors
MAPK1Mitogen-activated protein kinaseEffector-targeted signaling pathway
TLR4Pattern recognition receptorRecognition of microbial modulators
NLRP3Inflammasome sensorInflammatory modulation and tissue damage
SIRT1NAD-dependent deacetylaseAging-related physiological modulation
IGF1Growth factorAging and tissue homeostasis

How Is modulation of process of another organism Regulated?

GO:0035821 is regulated at multiple levels. The modulating organism controls effector expression in response to environmental cues such as temperature, pH, and host-derived signals. Host cells reciprocally regulate receptors, proteases, and ion channels that determine susceptibility to modulation. Inflammatory signaling through NF-kB and MAPK pathways can amplify or restrict effector-driven changes. Mechanotransduction via Piezo1 provides feedback between tissue stiffness and cellular responses during fibrosis. Aging-related pathways, including sirtuin and IGF-1 signaling, influence the baseline physiological state that modulates the outcome of cross-organism interactions.

modulation of process of another organism and Human Disease

GeneDisease / BiologyPotential Experimental Model
PIEZO1FibrosisKnockout and point-mutation human fibroblasts
AQP1Sepsis-associated fluid imbalanceKnockout epithelial cell lines
SCNN1ASodium homeostasis in sepsisKnock-in reporter cells
MMP9Tissue remodeling and inflammationOverexpression in macrophages
IL6Chronic inflammationKnockout and overexpression in immune cells
Infectious and Sepsis-Associated Modulation
Microbial effectors modulate host ion and water homeostasis, contributing to sepsis-associated organ dysfunction. Sodium imbalance and aquaporin dysregulation are documented features of sepsis, reflecting active modulation of host physiology. These changes can be measured by metabolomic and proteomic profiling of patient samples.
Fibrosis and Tissue Remodeling
Chronic modulation of extracellular matrix turnover leads to fibrosis in multiple organs. Matrix metalloproteinases and mechanosensitive channels such as Piezo1 are central to this process, and their activity can be targeted to limit pathological remodeling.
Chronic Inflammation and Aging
Persistent inflammatory modulation contributes to age-related tissue decline. Anti-inflammatory strategies, including bromelain, have been evaluated for their ability to reduce chronic inflammatory signaling. Aging itself is characterized by progressive physiological changes that alter susceptibility to modulation.

From modulation of process of another organism-Related Genes to Experimental Models

Research QuestionSuitable Model
Is a host gene required for microbial modulation?CRISPR knockout in human cell line
Does a specific point mutation alter susceptibility?CRISPR point mutation knock-in
Can a tagged effector be tracked in host cells?Tagged knock-in of effector gene
Does overexpression of a host factor enhance modulation?CRISPR overexpression cell model
Which host pathways are modulated at transcript level?RNA-seq of infected versus control cells
Which metabolites change during modulation?Metabolomics of host cells

How to Study the modulation of process of another organism Process

MethodWhat It MeasuresTypical Application
RNA-seqHost transcriptome changesInfection versus control
ProteomicsProtein abundance and modificationsEffector-target identification
MetabolomicsSmall-molecule profilesPhysiological shifts in infection
Confocal microscopyTissue morphology and matrix structureFibrosis and remodeling
ElectrophysiologyIon channel activitySodium and water transport
Cytokine assaysInflammatory mediator releaseChronic inflammation
CRISPR screeningHost genes required for modulationFunctional genomics
Transcriptomic Profiling
RNA-seq and microarray analysis compare host gene expression in the presence and absence of the modulating organism. This reveals pathways such as inflammatory signaling and ion transport that are altered during GO:0035821.
Proteomic and Metabolomic Analysis
Mass spectrometry-based proteomics and metabolomics quantify changes in host proteins and small molecules. These approaches have been used to characterize physiological shifts during infection and inflammation.
Imaging and Histology
Confocal and electron microscopy visualize morphological changes in host tissues, including extracellular matrix remodeling and cellular infiltration.
Functional Assays
Ion flux assays, barrier integrity tests, and cytokine measurements quantify physiological modulation. Aquaporin and sodium channel activity can be assessed using electrophysiology and fluorescent dyes.

How CRISPR Can Be Used to Study GO:0035821 modulation of process of another organism

Knockout

CRISPR knockout of candidate host genes in human cell lines enables testing whether a gene is required for microbial modulation. For example, knocking out PIEZO1 can reveal its role in fibrosis-associated mechanotransduction.

Point Mutation

Point-mutation knock-in models introduce specific amino acid changes to test structure-function relationships in host receptors or ion channels. This is useful for dissecting domains required for effector binding.

Knock-in

Tagged knock-in of effector or host genes allows tracking of protein localization and interactions during modulation. Fluorescent tags enable live-cell imaging of cross-organism interactions.

Overexpression

CRISPR overexpression models increase host gene dosage to test gain-of-function effects on susceptibility to modulation. Overexpressing inflammatory cytokines can amplify modulation phenotypes.

How EDITGENE Supports modulation of process of another organism Research

Researchers studying modulation of process of another organism-related genes often need to determine whether a candidate gene is causally involved in host susceptibility, effector delivery, or tissue remodeling. EDITGENE provides validated CRISPR models and bioinformatics support to accelerate this causal testing.
Contact EDITGENE today to design your custom CRISPR model for modulation of process of another organism research.

Frequently Asked Questions About modulation of process of another organism

It is a Gene Ontology biological process term describing a process in which one organism effects a change in a biological process in another organism, including changes to morphology, physiology, or signaling.
Genes encoding matrix metalloproteinases, ion channels, aquaporins, cytokines, and signaling kinases are commonly involved, including MMP2, MMP9, PIEZO1, AQP1, SCNN1A, IL6, and TNF.
Researchers use RNA-seq, proteomics, metabolomics, imaging, and CRISPR knockout or overexpression models to measure host changes during interaction with a modulating organism.
It provides a standardized way to annotate how pathogens alter host physiology, which is central to understanding sepsis, chronic infection, and tissue damage.
Examples include bacterial effectors that remodel extracellular matrix, viral proteins that alter host metabolism, and parasite factors that change ion homeostasis.
Sepsis, fibrosis, chronic inflammatory conditions, and aging-related tissue dysfunction have been linked to dysregulated cross-organism modulation.
Yes, CRISPR knockout, point mutation, knock-in, and overexpression models allow causal testing of host genes required for or resistant to modulation.
Piezo1 is a mechanosensitive ion channel that translates mechanical changes into cellular responses and has been implicated in fibrosis during tissue remodeling.
Aquaporins regulate water transport and are modulated during sepsis, contributing to fluid imbalance as part of host physiological changes.
Transcriptomics, proteomics, and metabolomics are commonly used to identify pathways altered during cross-organism interactions.

Conclusion

GO:0035821 modulation of process of another organism captures the diverse ways in which one organism alters the biology of another, from effector delivery to tissue remodeling and metabolic reprogramming. Its breadth makes it a powerful annotation for host-pathogen interaction studies and a framework for integrating multi-omics data. By combining CRISPR functional genomics with physiological readouts, researchers can identify causal host genes and pathways that drive disease-associated modulation. This knowledge supports the development of host-directed therapies for infection, inflammation, and fibrosis.

References

  1. 1. Naba A. 2024. Mechanisms of assembly and remodelling of the extracellular matrix.. Nat Rev Mol Cell Biol 25(11):865-885 PMID: 39223427
  2. 2. Wishart DS. 2019. Metabolomics for Investigating Physiological and Pathophysiological Processes.. Physiol Rev 99(4):1819-1875 PMID: 31434538
  3. 3. Bernal A et al.. 2023. Sodium Homeostasis, a Balance Necessary for Life.. Nutrients 15(2) PMID: 36678265
  4. 4. Khan SS et al.. 2017. Molecular and physiological manifestations and measurement of aging in humans.. Aging Cell 16(4):624-633 PMID: 28544158
  5. 5. Alves Nobre T et al.. 2025. Bromelain as a natural anti-inflammatory drug: a systematic review.. Nat Prod Res 39(5):1258-1271 PMID: 38676413
  6. 6. Lin Y et al.. 2025. Piezo1 and tissue fibrosis: insights into its role and potential for modulation.. Burns Trauma 13:tkaf054 PMID: 41245993
  7. 7. Rump K et al.. 2024. Aquaporins in sepsis- an update.. Front Immunol 15:1495206 PMID: 39544938
  8. 8. McIntyre JC et al.. 2017. Neuromodulation in Chemosensory Pathways.. Chem Senses 42(5):375-379 PMID: 28379355
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