GO:1901031 regulation of response to reactive oxygen species: Signaling Pathway, Genes, Functions and Research Methods

Research-grade guide for scientists and biopharma professionals

Key Takeaways

GO:1901031 (regulation of response to reactive oxygen species) is a biological process that modulates the frequency, rate or extent of cellular responses to reactive oxygen species (ROS).
ROS are not merely damaging agents; they act as signaling molecules in plant immunity, development, and stress responses, and their levels are tightly regulated [1,3,7].
Key regulators include plant hormones such as salicylic acid, which interacts with ROS signaling to orchestrate biotic stress responses.
Environmental stresses like cold, drought, and heat induce ROS accumulation and trigger adaptive transcriptional programs, including nuclear translocation of NAC transcription factors [4,5,6].
In mammals, ROS regulation impacts immune suppression by myeloid-derived suppressor cells and endothelial inflammation linked to ferroptosis [2,8].
CRISPR-based models (knockout, point mutation, knock-in, overexpression) enable causal dissection of ROS regulatory networks in plants and animals [1,5].

Description

Reactive oxygen species (ROS) are chemically reactive molecules containing oxygen, such as superoxide, hydrogen peroxide, and hydroxyl radicals. While historically viewed as harmful byproducts of metabolism, ROS are now recognized as essential signaling molecules that regulate growth, development, and stress responses [1,7]. The biological process termed regulation of response to reactive oxygen species (GO:1901031) encompasses any mechanism that modulates the frequency, rate, or extent of cellular responses to ROS. This regulation is critical for maintaining redox homeostasis and ensuring appropriate adaptive responses to environmental and developmental cues [3,6]. In plants, ROS signaling is intertwined with hormonal pathways, particularly salicylic acid, to coordinate defense against biotic stress. In mammals, dysregulated ROS responses contribute to inflammation, immune suppression, and cardiovascular disease [2,8]. Understanding the molecular players and regulatory logic of GO:1901031 is therefore central to both basic biology and translational research.

regulation of response to reactive oxygen species At A Glance

GO ID GO:1901031
GO term regulation of response to reactive oxygen species
Ontology biological_process
Synonym regulation of response to active oxygen species; regulation of response to AOS; regulation of response to reactive oxidative species; regulation of response to reactive oxygen intermediate; regulation of response to ROI; regulation of response to ROS
Major function Modulates the frequency, rate or extent of cellular responses to reactive oxygen species
Related processes ROS signaling, oxidative stress response, hormone signaling, immune suppression, ferroptosis
Key regulators Salicylic acid signaling, NAC transcription factors, NCOA4, MDSC-mediated immune suppression
Research relevance Target for improving stress tolerance in crops and treating inflammatory and cardiovascular diseases

What Is GO:1901031?

GO:1901031, regulation of response to reactive oxygen species, is defined as any process that modulates the frequency, rate or extent of a response to reactive oxygen species. In other words, it covers the cellular mechanisms that tune how cells sense, interpret, and react to ROS, ensuring that ROS signaling is balanced and context-appropriate.

Why Is regulation of response to reactive oxygen species Important in Cell Biology?

Regulation of ROS responses is fundamental to life because ROS can both damage macromolecules and serve as signals. Unchecked ROS responses lead to oxidative damage, while insufficient ROS signaling impairs defense and development [1,7]. In plants, fine-tuning ROS responses determines resistance to pathogens and tolerance to abiotic stresses such as cold, drought, and heat [1,4,5,6]. In mammals, ROS regulation influences immune cell function, inflammation, and diseases like atherosclerosis [2,8]. Thus, understanding GO:1901031 provides mechanistic insights into health, disease, and crop resilience.
Controls the balance between ROS-induced damage and ROS-mediated signaling.
Integrates with hormone pathways, notably salicylic acid, to coordinate plant immunity.
Enables adaptive responses to temperature extremes, drought, and other abiotic stresses [4,5,6].
Regulates photosynthetic electron transport to avoid excessive ROS generation.
Modulates immune suppression by myeloid-derived suppressor cells in cancer.
Impacts endothelial inflammation and ferroptosis in atherosclerosis.
Provides targets for crop improvement through genetic manipulation.
Offers therapeutic opportunities for inflammatory and cardiovascular diseases.
Essential for understanding redox biology across kingdoms.
Facilitates development of CRISPR-based models to dissect causal genes [1,5].

What Happens During regulation of response to reactive oxygen species?

ROS generation and perception
In simple terms: Cells first produce ROS and then sense them.
ROS are generated in various cellular compartments, including chloroplasts, mitochondria, and peroxisomes. In photosynthetic electron transport, regulation of ROS generation is critical to avoid photodamage. Plants and animals perceive ROS through redox-sensitive proteins, leading to activation of signaling cascades [1,7].
Signal transduction and hormone crosstalk
In simple terms: ROS signals are relayed through hormones and other messengers.
Salicylic acid signaling is intertwined with ROS to amplify defense responses against biotic stress. Other hormones, such as abscisic acid and ethylene, also modulate ROS responses under temperature stress. This crosstalk ensures a coordinated response to environmental challenges.
Transcriptional reprogramming
In simple terms: Cells change gene expression to cope with ROS.
Stress-induced nuclear translocation of transcription factors, such as ONAC023 in rice, activates multiple processes that improve drought and heat tolerance. These transcriptional changes lead to production of antioxidant enzymes and other protective proteins.
Feedback and resolution
In simple terms: The response is turned off when no longer needed.
To prevent excessive damage, ROS responses are attenuated by antioxidant systems and negative feedback loops. For example, regulation of ROS cellular targets is essential for proper plant development. In mammals, dysregulation of this feedback can lead to chronic inflammation.

Key Genes Involved in GO:1901031 regulation of response to reactive oxygen species

The following genes and proteins are key players in the regulation of response to reactive oxygen species, as supported by the cited literature.
GeneMajor RoleResearch Relevance
NCOA4Regulates ferritinophagy and ferroptosis, impacting endothelial inflammationTarget for atherosclerosis research
ONAC023Transcription factor that translocates to nucleus under stress, enhancing drought and heat toleranceCrop improvement via CRISPR
Salicylic acid pathway genes (e.g., ICS1, NPR1)Modulate ROS signaling in plant immunityBiotic stress resistance
MDSC-related genesRegulate ROS-mediated immune suppressionCancer immunotherapy
Photosynthetic electron transport componentsRegulate ROS generation during photosynthesisPhotosynthesis and stress studies
Antioxidant enzymes (e.g., SOD, CAT, APX)Detoxify ROS and modulate signalingStress tolerance mechanisms
NAC transcription factorsRegulate ROS-responsive gene expressionAbiotic stress tolerance
Hormone signaling genes (e.g., ABA, ethylene)Crosstalk with ROS under temperature stressClimate resilience
ROS target proteinsMediate developmental roles of ROSPlant development
Ferroptosis regulators (e.g., GPX4)Modulate lipid peroxidation and ROS responsesCell death pathways
Immune cell receptorsSense ROS and activate immune responsesInflammation research
Redox-sensitive kinasesTransduce ROS signalsSignal transduction
Chloroplast proteinsRegulate ROS production and signalingPhotosynthesis
Mitochondrial proteinsRegulate ROS generation and apoptosisCellular stress
Peroxisomal proteinsMetabolize ROS and lipidsMetabolic stress
Calcium channelsMediate ROS-induced calcium signalingStress signaling
MAPK cascade componentsTransmit ROS signals to transcription factorsDefense signaling

How Is regulation of response to reactive oxygen species Regulated?

The regulation of response to reactive oxygen species is itself controlled at multiple levels. In plants, salicylic acid signaling acts as a master regulator, intertwining with ROS to modulate defense gene expression. Environmental stresses such as cold, drought, and heat induce ROS accumulation and trigger transcriptional reprogramming via NAC transcription factors [4,5,6]. In mammals, NCOA4-mediated ferritinophagy regulates ferroptosis and endothelial inflammation, linking ROS responses to atherosclerosis. Additionally, myeloid-derived suppressor cells use ROS to suppress immune responses, a process that is tightly regulated in the tumor microenvironment.

regulation of response to reactive oxygen species and Human Disease

GeneDisease / BiologyPotential Experimental Model
NCOA4Atherosclerosis, endothelial inflammationKnockout mice, endothelial cell lines
MDSC-related genesCancer immune suppressionTumor models, co-culture systems
ONAC023Drought and heat sensitivity in riceRice knockout and overexpression lines
Salicylic acid pathway genesPlant immunityArabidopsis mutants, CRISPR knockouts
Photosynthetic ROS regulatorsPhotooxidative stressChloroplast transformation, mutants
Atherosclerosis and endothelial inflammation
NCOA4 is linked to endothelial cell ferritinophagy and ferroptosis, acting as a key regulator that aggravates aortic endothelial inflammation and atherosclerosis. Dysregulated ROS responses promote lipid peroxidation and inflammatory cytokine production, contributing to plaque formation.
Cancer and immune suppression
ROS act as regulators of myeloid-derived suppressor cell (MDSC)-mediated immune suppression. MDSCs produce ROS to inhibit T cell function, thereby promoting tumor progression. Targeting ROS regulatory pathways in MDSCs is a potential strategy for cancer immunotherapy.
Plant stress and crop loss
In plants, impaired regulation of ROS responses leads to reduced tolerance to biotic and abiotic stresses, causing yield losses [1,4,5,6]. For example, cold stress triggers ROS accumulation, and inadequate regulation can damage photosynthetic machinery. Understanding these mechanisms can guide breeding for climate-resilient crops.

From regulation of response to reactive oxygen species-Related Genes to Experimental Models

Research QuestionSuitable Model
Does NCOA4 regulate ferroptosis in endothelial cells?NCOA4 knockout endothelial cell line
What is the role of ONAC023 in drought tolerance?ONAC023 knockout and overexpression rice lines
How does salicylic acid modulate ROS signaling?Salicylic acid pathway mutants in Arabidopsis
What genes mediate MDSC ROS production?Knockout mice for candidate genes
How do photosynthetic proteins regulate ROS generation?Chloroplast mutants and point mutations
What is the impact of ROS on plant development?Tissue-specific overexpression lines

How to Study the regulation of response to reactive oxygen species Process

MethodWhat It MeasuresTypical Application
RNA-seqTranscriptional changesIdentify ROS-responsive genes
ROS imaging (DCFH-DA)Intracellular ROS levelsConfirm mutant phenotypes
Redox proteomicsProtein oxidationDiscover ROS targets
CRISPR library screeningGene function at scaleFind regulators of ROS responses
Western blotProtein expression and modificationValidate signaling changes
qPCRGene expressionQuantify specific transcripts
ChIP-seqTranscription factor bindingMap ONAC023 targets
MetabolomicsMetabolite levelsAssess oxidative stress
Transcriptomics and RNA-seq
RNA sequencing can identify global transcriptional changes in response to ROS or in mutants of regulatory genes. For example, stress-induced nuclear translocation of ONAC023 was linked to altered expression of multiple stress-responsive genes. Comparative RNA-seq of wild-type and knockout lines reveals pathways controlled by GO:1901031 regulators.
ROS detection and imaging
Fluorescent probes such as DCFH-DA and Amplex Red measure ROS levels in live cells. Imaging ROS dynamics in plant and animal tissues helps localize ROS production and response [3,7]. These methods are essential to confirm that genetic perturbations alter ROS responses.
Proteomics and redox proteomics
Mass spectrometry-based proteomics identifies proteins with oxidized cysteine residues, revealing ROS targets and signaling nodes. Redox proteomics can quantify changes in oxidation state upon genetic manipulation of regulatory genes.
Genetic screens and CRISPR libraries
CRISPR knockout libraries enable unbiased discovery of genes that regulate ROS responses. For instance, screens in plant or mammalian cells can identify modifiers of ROS-induced phenotypes [1,5]. These screens are powerful for annotating GO:1901031 components.

How CRISPR Can Be Used to Study GO:1901031 regulation of response to reactive oxygen species

Knockout

CRISPR knockout of candidate genes such as NCOA4 or ONAC023 can reveal their causal role in regulating ROS responses. For example, NCOA4 knockout reduces ferroptosis and endothelial inflammation, while ONAC023 knockout in rice impairs drought and heat tolerance.

Point Mutation

Introducing precise point mutations in genes encoding redox-sensitive proteins can dissect specific phosphorylation or oxidation sites. This approach helps determine which residues are critical for ROS signaling.

Knock-in

Knock-in of tagged versions of proteins (e.g., GFP, HA) allows visualization and purification of ROS regulatory complexes. Tagged ONAC023 can be used to track nuclear translocation under stress.

Overexpression

Overexpression of antioxidant enzymes or regulatory transcription factors can enhance ROS tolerance. For instance, overexpressing ONAC023 improves drought and heat tolerance in rice. Overexpression models are useful for gain-of-function studies.

How EDITGENE Supports regulation of response to reactive oxygen species Research

Researchers studying regulation of response to reactive oxygen species-related genes often need to determine whether a candidate gene is causally involved in ROS signaling, stress tolerance, or disease. EDITGENE provides comprehensive CRISPR services to generate precisely engineered cell and animal models, accelerating functional validation and therapeutic development.
Contact EDITGENE today to design your custom CRISPR model for regulation of response to reactive oxygen species research.

Frequently Asked Questions About regulation of response to reactive oxygen species

GO:1901031 is the Gene Ontology term for regulation of response to reactive oxygen species, defined as any process that modulates the frequency, rate or extent of a response to reactive oxygen species.
Key genes include NCOA4, ONAC023, salicylic acid pathway genes, MDSC-related genes, and antioxidant enzymes, as shown in plant and mammalian studies [1,2,5,8].
Salicylic acid signaling intertwines with ROS to amplify defense responses against biotic stress in plants.
NCOA4 regulates ferritinophagy and ferroptosis, aggravating endothelial inflammation and atherosclerosis.
Cold stress induces ROS accumulation, and plants activate molecular and physiological adaptive mechanisms to regulate ROS responses.
ONAC023 translocates to the nucleus under stress and improves drought and heat tolerance through multiple processes in rice.
Photosynthetic electron transport generates ROS, and its regulation is critical to avoid photodamage.
Methods include RNA-seq, ROS imaging, redox proteomics, and CRISPR library screening [1,3,7].
ROS produced by myeloid-derived suppressor cells regulate immune suppression in the tumor microenvironment.
Yes, CRISPR knockout, point mutation, knock-in, and overexpression models enable causal dissection of ROS regulatory genes [1,2,5].

Conclusion

GO:1901031, regulation of response to reactive oxygen species, is a central biological process that integrates ROS signaling with hormonal, transcriptional, and metabolic pathways. Its dysregulation contributes to plant stress susceptibility and human diseases such as atherosclerosis and cancer. The genes and mechanisms highlighted here provide a foundation for further research. EDITGENE offers advanced CRISPR services to facilitate functional studies and therapeutic development targeting this process.

References

  1. 1. Lukan T et al.. 2022. Intertwined Roles of Reactive Oxygen Species and Salicylic Acid Signaling Are Crucial for the Plant Response to Biotic Stress.. Int J Mol Sci 23(10) PMID: 35628379
  2. 2. Zhu L et al.. 2025. NCOA4 linked to endothelial cell ferritinophagy and ferroptosis:a key regulator aggravate aortic endothelial inflammation and atherosclerosis.. Redox Biol 79:103465 PMID: 39700692
  3. 3. Krieger-Liszkay A et al.. 2022. Regulation of the generation of reactive oxygen species during photosynthetic electron transport.. Biochem Soc Trans 50(2):1025-1034 PMID: 35437580
  4. 4. Feng Y et al.. 2025. Plant Coping with Cold Stress: Molecular and Physiological Adaptive Mechanisms with Future Perspectives.. Cells 14(2) PMID: 39851537
  5. 5. Chang Y et al.. 2024. Stress-induced nuclear translocation of ONAC023 improves drought and heat tolerance through multiple processes in rice.. Nat Commun 15(1):5877 PMID: 38997294
  6. 6. Devireddy AR et al.. 2021. Role of Reactive Oxygen Species and Hormones in Plant Responses to Temperature Changes.. Int J Mol Sci 22(16) PMID: 34445546
  7. 7. Singh VP et al.. 2024. Evolution of reactive oxygen species cellular targets for plant development.. Trends Plant Sci 29(8):865-877 PMID: 38519324
  8. 8. Ohl K et al.. 2018. Reactive Oxygen Species as Regulators of MDSC-Mediated Immune Suppression.. Front Immunol 9:2499 PMID: 30425715
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