GO:0002679 respiratory burst involved in defense response: Oxidative Defense Pathway, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0002679 describes a defense-associated phase of elevated oxygen consumption that produces hydrogen peroxide, superoxide anions and hydroxyl radicals through an NADH-dependent system.
• The respiratory burst is best characterized in phagocytes, where it supports host defense against ingested microorganisms.
• In alveolar macrophages, respiratory burst-derived reactive oxygen species also act in signal transduction, linking oxidative chemistry to immune gene regulation.
• Neutrophil respiratory burst activity is modulated by physiological stress such as exercise and by mitochondrial permeability transition pore behavior.
• The process is evolutionarily conserved: respiratory burst oxidase homolog (Rboh) genes operate in plants, and comparable oxidative responses occur in invertebrates.
• Researchers study GO:0002679 with phagocyte functional assays, ROS detection, gene knockout and genome-wide screens to define causal genes and defense mechanisms.
Description
GO:0002679, respiratory burst involved in defense response, is a biological process in which a cell undergoes a phase of elevated metabolic activity and increased oxygen consumption as part of a defense response, leading to production of hydrogen peroxide (H2O2), superoxide anions and hydroxyl radicals by an NADH-dependent system. This process is classically associated with phagocytes, where it provides reactive oxygen species (ROS) that participate in host defense. The same oxidative chemistry also has signaling roles, as shown in alveolar macrophages where respiratory burst contributes to signal transduction. Because the term is defined by both metabolic output and defensive context, it is relevant to immunology, host-pathogen interaction, redox biology and comparative physiology. The respiratory burst is not restricted to mammalian phagocytes. In plants, respiratory burst oxidase homolog (Rboh) genes encode NADPH oxidase components that generate ROS during defense and developmental processes, and genome-wide analyses have identified Rboh family members in Aquilaria species. In tomato roots, inoculation with Pochonia chlamydosporia triggers a defense response that affects parasitism by Meloidogyne javanica, illustrating how defense-associated oxidative responses are studied in plant-pathogen systems. In invertebrates, miR-210 modulates respiratory burst in Apostichopus japonicus coelomocytes via targeting Toll-like receptor, showing conserved regulatory logic between innate immune signaling and ROS production. For researchers, GO:0002679 provides a precise annotation target for experiments that measure oxygen consumption, ROS generation and defense outcomes. The process intersects with neutrophil degranulation and exercise-induced alterations in respiratory burst activity, with mitochondrial permeability transition pore involvement in oxidative burst and NETosis, and with micronutrient deficiency-induced oxidative stress in plants. These connections make GO:0002679 a useful framework for comparing defense-associated oxidative mechanisms across cell types and species.
respiratory burst involved in defense response At A Glance
| GO ID | GO:0002679 |
|---|---|
| GO term | respiratory burst involved in defense response |
| Ontology | biological_process |
| Synonym | none listed in QuickGO |
| Major function | Defense-associated increase in oxygen consumption leading to production of H2O2, superoxide anions and hydroxyl radicals by an NADH-dependent system |
| Representative cell types | Phagocytes such as neutrophils and alveolar macrophages |
| Conserved systems | Plant Rboh-dependent oxidative responses and invertebrate coelomocyte respiratory burst |
| Related physiological context | Exercise-induced alterations in neutrophil respiratory burst and mitochondrial permeability transition pore involvement in oxidative burst |
| Related stress context | Micronutrient deficiency-induced oxidative stress in plants |
What Is GO:0002679?
In this article, GO:0002679 is understood as a defense-related phase of increased metabolic activity in which oxygen consumption rises and an NADH-dependent system produces hydrogen peroxide (H2O2), superoxide anions and hydroxyl radicals. The term emphasizes both the metabolic burst and its defensive purpose, rather than ROS production in isolation. It is therefore broader than a single enzyme reaction and can be applied to phagocyte host defense as well as to conserved defense-associated oxidative responses in other systems.
Why Is respiratory burst involved in defense response Important in Cell Biology?
GO:0002679 is important because it connects a measurable metabolic event, increased oxygen consumption, to a defined defensive outcome, production of H2O2, superoxide anions and hydroxyl radicals by an NADH-dependent system. This makes the term useful for interpreting host defense experiments in phagocytes and for comparing defense-associated oxidative responses across plants and animals. It also provides a conceptual bridge between innate immune signaling, mitochondrial behavior and redox regulation, as illustrated by studies of alveolar macrophage signal transduction, neutrophil NETosis and exercise-related neutrophil changes.
• Provides a precise annotation for defense-associated oxygen consumption and ROS production by an NADH-dependent system.
• Supports mechanistic studies of phagocyte host defense against microorganisms.
• Links respiratory burst chemistry to signal transduction in alveolar macrophages.
• Connects neutrophil biology to degranulation and physiological stress such as exercise.
• Includes mitochondrial permeability transition pore involvement in oxidative burst and NETosis.
• Has conserved plant counterparts through Rboh genes and defense-associated ROS.
• Is modulated by immune-related microRNAs such as miR-210 in invertebrate coelomocytes.
• Intersects with oxidative stress caused by micronutrient deficiency in plants.
• Offers a comparative framework for studying innate immunity across species.
• Guides design of knockout, knock-in and overexpression experiments to test causal genes in defense responses.
What Happens During respiratory burst involved in defense response?
Defense-triggered metabolic activation
In simple terms: The cell switches into a high-energy defensive mode when it detects a threat.
GO:0002679 begins with a defense response that drives a phase of elevated metabolic activity and increased oxygen consumption. In phagocytes, this activation is part of host defense against microorganisms. In alveolar macrophages, respiratory burst activity is also connected to signal transduction, indicating that the metabolic activation is integrated with immune signaling rather than being only a terminal effector event. In plants, defense responses triggered by inoculation with Pochonia chlamydosporia affect parasitism by Meloidogyne javanica, showing that defense-associated metabolic reprogramming occurs in plant roots as well.
NADH-dependent production of reactive oxygen species
In simple terms: An NADH-dependent system converts oxygen into reactive molecules that help fight infection.
The defining output of GO:0002679 is production of hydrogen peroxide (H2O2), superoxide anions and hydroxyl radicals by an NADH-dependent system. This chemistry is the core of the respiratory burst and explains why the process is measured through oxygen consumption and ROS detection. In plants, respiratory burst oxidase homolog (Rboh) genes are associated with ROS-mediated metabolite biosynthesis and resin deposition, demonstrating that NADPH/Rboh-type oxidative systems participate in defense-linked outputs beyond direct killing. In animal coelomocytes, miR-210 modulates respiratory burst via targeting Toll-like receptor, linking innate immune receptor regulation to ROS production.
Integration with phagocyte effector functions
In simple terms: The oxidative burst works together with other immune weapons such as granule release and NET formation.
Respiratory burst activity in neutrophils is studied alongside degranulation, and exercise-induced alterations in neutrophil degranulation and respiratory burst activity suggest coordinated regulation of these effector functions. The mitochondrial permeability transition pore is involved in oxidative burst and NETosis of human neutrophils, indicating that mitochondrial behavior contributes to the oxidative burst program and to neutrophil extracellular trap formation. These findings place GO:0002679 within a broader effector network rather than as an isolated ROS-producing reaction.
Conserved defense-associated oxidative responses
In simple terms: Similar oxidative defense strategies appear in plants and invertebrates, not only in human immune cells.
Genome-wide analysis of respiratory burst oxidase homolog (Rboh) genes in Aquilaria species provides insight into ROS-mediated metabolite biosynthesis and resin deposition, showing conservation of Rboh-based oxidative defense machinery in plants. In tomato roots, Pochonia chlamydosporia inoculation triggers a defense response that affects parasitism by Meloidogyne javanica, illustrating experimental dissection of defense-associated oxidative responses in a plant-pathogen system. In Apostichopus japonicus, miR-210 modulates respiratory burst in coelomocytes via targeting Toll-like receptor, demonstrating that invertebrate innate immune cells also regulate respiratory burst through conserved signaling components. Micronutrient deficiency-induced oxidative stress in plants further shows how nutritional status can intersect with oxidative defense pathways.
Key Genes Involved in GO:0002679 respiratory burst involved in defense response
The following genes and gene families are recurrently associated with respiratory burst involved in defense response across phagocyte, invertebrate and plant systems in the cited literature.
| Gene | Major Role | Research Relevance |
|---|---|---|
| Toll-like receptor (invertebrate coelomocyte context) | Innate immune receptor targeted by miR-210 during modulation of respiratory burst | Tests how microRNA-receptor axes control respiratory burst in coelomocytes |
| miR-210 | Modulates respiratory burst by targeting Toll-like receptor in Apostichopus japonicus coelomocytes | Provides a regulatory node for perturbing respiratory burst in invertebrate immunity |
| Rboh family (respiratory burst oxidase homologs) | Plant NADPH oxidase homologs associated with ROS-mediated metabolite biosynthesis and resin deposition | Supports genome-wide and functional studies of oxidative defense in plants |
| Mitochondrial permeability transition pore components | Involved in oxidative burst and NETosis of human neutrophils | Links mitochondrial physiology to neutrophil oxidative burst and NET formation |
| Neutrophil degranulation machinery | Coordinated with respiratory burst activity and altered by exercise | Enables studies of effector function coupling in neutrophils |
| Alveolar macrophage signaling components | Participate in respiratory burst-associated signal transduction | Supports mechanistic work on ROS-dependent immune signaling |
| Phagocyte NADH-dependent oxidase system | Produces H2O2, superoxide anions and hydroxyl radicals during defense | Core functional target for respiratory burst assays |
| Plant defense response genes (tomato root context) | Triggered by Pochonia chlamydosporia inoculation and affect Meloidogyne javanica parasitism | Provides a plant pathosystem for defense-associated oxidative responses |
| Micronutrient stress-responsive genes (plant context) | Associated with micronutrient deficiency-induced oxidative stress | Connects nutritional status to oxidative defense research |
| Neutrophil effector genes | Underlie degranulation and respiratory burst changes after exercise | Supports exercise immunology studies of neutrophil function |
| NETosis-associated genes | Function in oxidative burst-linked neutrophil extracellular trap formation | Enables dissection of oxidative burst versus NETosis contributions |
| Macrophage signal transduction genes | Mediate respiratory burst-dependent signaling in alveolar macrophages | Supports studies of ROS as second messengers in immunity |
| Invertebrate coelomocyte immune genes | Regulate respiratory burst in Apostichopus japonicus coelomocytes | Provides comparative innate immunity models |
| Aquilaria Rboh genes | Implicated in ROS-mediated metabolite biosynthesis and resin deposition | Supports genome-wide analysis of Rboh gene families |
| Tomato root defense genes | Respond to Pochonia chlamydosporia inoculation and influence nematode parasitism | Enables plant defense priming experiments |
| Plant oxidative stress response genes | Respond to micronutrient deficiency-induced oxidative stress | Links nutrient stress to oxidative defense pathways |
How Is respiratory burst involved in defense response Regulated?
Respiratory burst involved in defense response is regulated at multiple levels. In invertebrate coelomocytes, miR-210 modulates respiratory burst by targeting Toll-like receptor, placing microRNA control upstream of innate immune receptor signaling. In human neutrophils, the mitochondrial permeability transition pore is involved in oxidative burst and NETosis, indicating that mitochondrial permeability transition contributes to regulation of the oxidative burst program. Physiological state also regulates the process: exercise induces alterations in neutrophil degranulation and respiratory burst activity, suggesting that systemic stress and exercise-related signals modify respiratory burst capacity. In alveolar macrophages, respiratory burst participates in signal transduction, which implies feedback between ROS production and signaling pathways that may shape the magnitude and duration of the response. In plants, micronutrient deficiency-induced oxidative stress and Rboh-dependent ROS production indicate that nutritional and defense-related cues can regulate oxidative responses.
respiratory burst involved in defense response and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| Toll-like receptor / miR-210 axis | Innate immune regulation of respiratory burst in invertebrate coelomocytes | Coelomocyte knockdown or overexpression of miR-210 and Toll-like receptor |
| Mitochondrial permeability transition pore components | Neutrophil oxidative burst and NETosis | Human neutrophil assays with permeability transition pore perturbation |
| Rboh family genes | Plant ROS-mediated metabolite biosynthesis and resin deposition | Genome-wide Rboh analysis and plant knockout lines |
| Tomato root defense genes | Defense response affecting Meloidogyne javanica parasitism | Pochonia chlamydosporia inoculation in tomato root systems |
| Phagocyte NADH-dependent oxidase system | Host defense against microorganisms | Phagocyte functional assays and ROS detection |
Infectious disease and impaired host defense
The respiratory burst of phagocytes is a component of host defense, and its role in defense against microorganisms is central to understanding why defects or dysregulation of this process can compromise antimicrobial immunity. Alveolar macrophage respiratory burst also contributes to signal transduction, so altered regulation may affect lung immune responses beyond direct killing. Neutrophil respiratory burst and degranulation are modulated by exercise, which is relevant to how physiological stress may influence susceptibility to infection.
Neutrophil-driven inflammatory pathology and NETosis
The mitochondrial permeability transition pore is involved in oxidative burst and NETosis of human neutrophils, linking respiratory burst biology to neutrophil extracellular trap formation. Because NETosis is associated with inflammatory and thrombotic pathology, this connection makes GO:0002679 relevant to research on neutrophil-mediated tissue injury and inflammatory disease mechanisms. Exercise-induced changes in neutrophil degranulation and respiratory burst activity further indicate that the process is sensitive to physiological context.
Plant disease and crop defense
In tomato roots, inoculation with Pochonia chlamydosporia triggers a defense response that affects parasitism by Meloidogyne javanica, providing a model for how defense-associated oxidative responses influence plant disease outcomes. Rboh genes in Aquilaria species are linked to ROS-mediated metabolite biosynthesis and resin deposition, showing that oxidative defense machinery can also shape specialized plant products. Micronutrient deficiency-induced oxidative stress in plants demonstrates that nutritional imbalance can interact with oxidative defense pathways relevant to crop health.
From respiratory burst involved in defense response-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Is a candidate gene required for respiratory burst during defense? | CRISPR knockout in a phagocyte or relevant defense cell model |
| Does a specific point mutation alter oxidative burst capacity? | CRISPR point-mutation knock-in in the endogenous locus |
| Can a tagged oxidase component be tracked during burst activation? | Tagged knock-in for imaging and proteomics |
| Does overexpression of a regulatory RNA change respiratory burst? | Overexpression of miR-210 or related regulators in coelomocytes |
| Which Rboh family members contribute to defense-associated ROS? | Plant genome-wide Rboh analysis with knockout or overexpression lines |
| Does a defense trigger alter oxidative responses in roots? | Tomato root inoculation with Pochonia chlamydosporia |
How to Study the respiratory burst involved in defense response Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Oxygen consumption assay | Elevated metabolic activity and oxygen uptake during respiratory burst | Phagocyte defense experiments |
| ROS detection (H2O2, superoxide, hydroxyl radicals) | Production of reactive oxygen species by an NADH-dependent system | Core respiratory burst phenotyping |
| Neutrophil degranulation assay | Coordinated effector function with respiratory burst | Exercise immunology and neutrophil studies |
| Mitochondrial permeability transition and NETosis assays | Mitochondrial involvement in oxidative burst and NET formation | Human neutrophil mechanism studies |
| Genome-wide Rboh analysis | Identification and classification of respiratory burst oxidase homologs | Plant defense and specialized metabolism research |
| miR-210 / Toll-like receptor perturbation | Regulatory control of respiratory burst in coelomocytes | Invertebrate innate immunity studies |
| Plant inoculation and parasitism scoring | Defense response and nematode parasitism outcomes | Tomato root-Pochonia chlamydosporia-Meloidogyne javanica system |
| Oxidative stress marker measurement | Micronutrient deficiency-induced oxidative stress | Plant nutrition and redox studies |
Measuring oxygen consumption and ROS production
Because GO:0002679 is defined by increased oxygen consumption and production of H2O2, superoxide anions and hydroxyl radicals by an NADH-dependent system, direct measurement of oxygen consumption and ROS species is a core method. In phagocyte studies, respiratory burst activity is assessed alongside degranulation to capture coordinated effector functions. In neutrophils, oxidative burst measurements are combined with NETosis readouts to distinguish overlapping processes.
Genetic perturbation and genome-wide analysis
Genome-wide analysis of respiratory burst oxidase homolog (Rboh) genes in Aquilaria species demonstrates how gene family discovery can be coupled to ROS-mediated phenotypes. In invertebrate systems, targeting Toll-like receptor with miR-210 provides a genetic approach to modulate respiratory burst in coelomocytes. In plant pathosystems, inoculation experiments with Pochonia chlamydosporia and Meloidogyne javanica allow defense response phenotypes to be linked to oxidative mechanisms.
Signal transduction and mitochondrial readouts
Respiratory burst in alveolar macrophages has been studied as a signal transduction phenomenon, requiring methods that connect ROS production to downstream signaling. In human neutrophils, mitochondrial permeability transition pore involvement in oxidative burst and NETosis requires mitochondrial function assays combined with oxidative burst measurements. Exercise immunology studies measure neutrophil degranulation and respiratory burst activity before and after exercise to define physiological regulation.
Oxidative stress context in plants
Micronutrient deficiency-induced oxidative stress in plants provides a framework for measuring oxidative damage and defense-related redox changes under nutritional stress. Rboh gene expression and ROS-mediated metabolite or resin deposition can be used as readouts of defense-associated oxidative activity in Aquilaria. Tomato root defense responses triggered by Pochonia chlamydosporia offer a pathosystem in which oxidative defense and nematode parasitism can be scored together.
How CRISPR Can Be Used to Study GO:0002679 respiratory burst involved in defense response
Knockout
CRISPR knockout is used to test whether a candidate gene is required for respiratory burst involved in defense response. Because the process is defined by defense-associated oxygen consumption and production of H2O2, superoxide anions and hydroxyl radicals by an NADH-dependent system, knocking out a suspected oxidase or signaling component allows direct assessment of its contribution. In neutrophils, knockout approaches can help separate oxidative burst from NETosis when mitochondrial permeability transition pore components are targeted. In plants, knockout of Rboh family members can be used to test their roles in ROS-mediated metabolite biosynthesis and resin deposition.
Point Mutation
CRISPR point mutation enables fine mapping of residues that control respiratory burst activity without eliminating the entire protein. This is valuable when studying defense-associated oxidative signaling, where partial loss or gain of function may better model physiological regulation than complete knockout. For example, point mutations can be introduced into components linked to mitochondrial permeability transition pore involvement in oxidative burst and NETosis to test which domains are required. In invertebrate systems, point mutation of Toll-like receptor residues can be combined with miR-210 perturbation to dissect regulatory interactions.
Knock-in
Knock-in strategies allow tagging or reporter insertion at endogenous loci to track respiratory burst components in real time. Tagged knock-in of oxidase or signaling proteins supports imaging and proteomic analysis of the defense-associated oxidative burst. In plant systems, knock-in reporters for Rboh genes can be used to monitor ROS-mediated processes such as metabolite biosynthesis and resin deposition. In neutrophils, knock-in of reporters linked to mitochondrial permeability transition pore components can help visualize oxidative burst and NETosis dynamics.
Overexpression
Overexpression is used to test whether increasing the level of a regulator enhances or suppresses respiratory burst. Overexpression of miR-210 modulates respiratory burst in Apostichopus japonicus coelomocytes via targeting Toll-like receptor, demonstrating that gain-of-function approaches can reveal regulatory control. In plant systems, overexpression of Rboh genes can be used to probe ROS-mediated metabolite biosynthesis and resin deposition. In phagocyte models, overexpression of signaling components can test whether respiratory burst-associated signal transduction is amplified.
How EDITGENE Supports respiratory burst involved in defense response Research
Researchers studying respiratory burst involved in defense response-related genes often need to determine whether a candidate gene is causally involved in defense-associated oxygen consumption and ROS production, or whether it merely correlates with the phenotype. Establishing causality requires controlled genetic perturbation in relevant cell models, followed by functional readouts of H2O2, superoxide and hydroxyl radical production. Because the process spans phagocyte host defense, neutrophil NETosis, invertebrate innate immunity and plant Rboh-dependent oxidative responses, experimental systems must be matched to the biological context.
Contact EDITGENE today to design your custom CRISPR model for respiratory burst involved in defense response research.
Frequently Asked Questions About respiratory burst involved in defense response
What is respiratory burst involved in defense response (GO:0002679)?
It is a biological process defined as a defense-associated phase of elevated metabolic activity with increased oxygen consumption, leading to production of hydrogen peroxide, superoxide anions and hydroxyl radicals by an NADH-dependent system.
What genes are involved in respiratory burst involved in defense response?
Genes and systems implicated in the cited literature include Toll-like receptor and miR-210 in invertebrate coelomocytes, Rboh family genes in plants, mitochondrial permeability transition pore components in neutrophils, and phagocyte NADH-dependent oxidase components.
Why is respiratory burst important for host defense?
The respiratory burst of phagocytes contributes to host defense against microorganisms through production of reactive oxygen species. In alveolar macrophages, it also participates in signal transduction.
How is respiratory burst measured in the laboratory?
It is measured by oxygen consumption and detection of H2O2, superoxide anions and hydroxyl radicals, often alongside degranulation or NETosis readouts in phagocyte studies.
Does exercise affect neutrophil respiratory burst?
Yes, exercise-induced alterations in neutrophil degranulation and respiratory burst activity have been described, indicating physiological regulation of this process.
What is the role of mitochondria in respiratory burst?
The mitochondrial permeability transition pore is involved in oxidative burst and NETosis of human neutrophils, linking mitochondrial function to the oxidative burst program.
Do plants have a respiratory burst involved in defense response?
Plant systems use respiratory burst oxidase homolog (Rboh) genes for ROS-mediated processes, and defense responses in tomato roots can be triggered by Pochonia chlamydosporia inoculation.
How does miR-210 regulate respiratory burst?
miR-210 modulates respiratory burst in Apostichopus japonicus coelomocytes via targeting Toll-like receptor.
What is the difference between respiratory burst and NETosis?
Respiratory burst refers to defense-associated oxygen consumption and ROS production, while NETosis is neutrophil extracellular trap formation; mitochondrial permeability transition pore involvement connects the two processes.
How can CRISPR help study GO:0002679?
CRISPR knockout, point mutation, knock-in and overexpression models allow causal testing of candidate genes in defense-associated ROS production and related phenotypes such as NETosis or plant defense responses.
Conclusion
GO:0002679, respiratory burst involved in defense response, defines a defense-associated metabolic burst in which oxygen consumption increases and an NADH-dependent system produces hydrogen peroxide, superoxide anions and hydroxyl radicals. Its relevance extends from phagocyte host defense and alveolar macrophage signaling to neutrophil NETosis, invertebrate coelomocyte regulation by miR-210, and plant Rboh-dependent oxidative responses. Because the process is measurable through oxygen consumption and ROS detection, it is well suited to genetic perturbation studies that establish causality. Researchers can advance the field by combining functional assays with CRISPR-based knockout, point-mutation, knock-in and overexpression models, and by using library screening and bioinformatics to identify new regulators. Such work will clarify how defense-associated oxidative bursts are controlled across cell types and species, and how they contribute to immunity, inflammation and plant defense.
References
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- 2. Gupta R et al.. 2024. Micronutrient deficiency-induced oxidative stress in plants.. Plant Cell Rep 43(9):213 PMID: 39133336
- 3. Peake JM. 2002. Exercise-induced alterations in neutrophil degranulation and respiratory burst activity: possible mechanisms of action.. Exerc Immunol Rev 8:49-100 PMID: 12690938
- 4. Vorobjeva N et al.. 2020. Mitochondrial permeability transition pore is involved in oxidative burst and NETosis of human neutrophils.. Biochim Biophys Acta Mol Basis Dis 1866(5):165664 PMID: 31926265
- 5. Begum K et al.. 2023. Genome-wide analysis of respiratory burst oxidase homolog (Rboh) genes in Aquilaria species and insight into ROS-mediated metabolites biosynthesis and resin deposition.. Front Plant Sci 14:1326080 PMID: 38405033
- 6. Li C et al.. 2016. miR210 modulates respiratory burst in Apostichopus japonicus coelomocytes via targeting Toll-like receptor.. Dev Comp Immunol 65:377-381 PMID: 27545641
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- 8. Gouveia AS et al.. 2023. Inoculation of Pochonia chlamydosporia triggers a defense response in tomato roots, affecting parasitism by Meloidogyne javanica.. Microbiol Res 266:127242 PMID: 36356349
