GO:0010225 response to UV-C: Cellular Stress Response, Genes, Functions and Research Methods

Research-grade guide for scientists and biopharma professionals

Key Takeaways

GO:0010225 (response to UV-C) describes any cellular or organismal change triggered by UV-C radiation (100-280 nm), including gene expression, metabolic and structural adjustments [1,4,5].
UV-C is a potent DNA-damaging agent and is widely used to study DNA repair, oxidative stress and cell death pathways in human fibroblasts and plants [5,4].
In plants, UV-C triggers delayed ripening and alters cell wall and metabolic profiles in fruits such as peach and sweet cherry [1,7,8].
UV-C also induces systemic metabolic responses, including ureide accumulation in Arabidopsis leaves, that overlap with wounding responses.
UV-C disinfection technology is an applied outcome of understanding UV-C responses, used for air and surface decontamination [3,6].
Key experimental approaches include transcriptomics, cellular fractionation, metabolic profiling and CRISPR-based gene editing to dissect UV-C response pathways [5,1,4].

Description

Response to UV-C (GO:0010225) is a biological process that encompasses the changes in cell state or activity caused by exposure to UV-C radiation, which spans wavelengths from 100 to 280 nm. This high-energy ultraviolet range is strongly absorbed by nucleic acids and proteins, making it a powerful tool for studying stress responses, DNA damage and repair, and cellular adaptation [5,4]. The term is defined in QuickGO as any process that results in a change in state or activity of a cell or an organism as a result of a UV-C radiation stimulus. Researchers use UV-C as a controlled environmental cue to probe signaling cascades, gene expression reprogramming and metabolic shifts in organisms ranging from plants to humans [1,5,4]. Understanding this response is critical for both fundamental biology and applied fields such as food preservation and disinfection technology [7,3,6].

response to UV-C At A Glance

GO ID GO:0010225
GO term response to UV-C
Ontology biological_process
Synonym response to germicidal ultraviolet light stimulus; response to shortwave ultraviolet radiation stimulus; response to UV-C light stimulus
Major function Cellular and organismal response to UV-C radiation (100-280 nm), including gene expression, metabolic and structural changes
Related stimuli UV-C radiation, germicidal ultraviolet light
Taxonomic range Across eukaryotes and prokaryotes, including plants and humans
Key experimental readouts Transcriptomics, metabolomics, cell wall analysis, DNA damage assays

What Is GO:0010225?

GO:0010225 response to UV-C refers to the sum of cellular and organismal changes triggered by UV-C light (100-280 nm). This includes alterations in gene expression, enzyme production, metabolic pathways, cell wall properties and physiological outcomes such as delayed ripening or cell death. The term captures both immediate stress signaling and longer-term adaptive or damaging effects [1,4,5].

Why Is response to UV-C Important in Cell Biology?

Response to UV-C is important because UV-C is both a ubiquitous environmental stressor and a widely used experimental and industrial tool. In humans, UV-C exposure causes DNA damage and triggers complex transcriptional and metabolic responses that are relevant to cancer and cell death. In agriculture, UV-C treatment is used to extend shelf life and modulate ripening, with direct implications for postharvest quality [1,7,8]. In public health, UV-C disinfection systems rely on understanding how UV-C inactivates pathogens and how biological systems respond to it [3,6]. Thus, GO:0010225 bridges fundamental stress biology with applied biotechnology.
UV-C is a major DNA-damaging agent used to study DNA repair and cell death pathways.
UV-C triggers delayed ripening in fruits, affecting postharvest quality and shelf life.
UV-C alters cell wall composition and metabolism in conifer needles and fruits [2,8].
UV-C induces ureide accumulation in Arabidopsis, linking to nitrogen metabolism.
UV-C disinfection is used in clinical and public settings to inactivate airborne pathogens [3,6].
UV-C responses overlap with wounding and other stress pathways, revealing crosstalk.
Transcriptomic and cellular fractionation studies reveal compartment-specific UV-C responses.
UV-C treatment can modulate antioxidant capacity in fruits, with nutritional implications.
Understanding UV-C response aids development of UV-C-based therapies and sterilization.
CRISPR screens can identify genes required for UV-C survival, linking genotype to phenotype.

What Happens During response to UV-C?

UV-C perception and immediate damage
In simple terms: UV-C light hits the cell and directly damages DNA and other molecules.
UV-C radiation (100-280 nm) is absorbed by nucleic acids, causing lesions such as cyclobutane pyrimidine dimers. In human fibroblasts, UV-C irradiation leads to rapid changes in transcript localization and stress signaling. In plants, UV-C triggers early metabolic shifts, including ureide accumulation in Arabidopsis leaves.
Transcriptional reprogramming
In simple terms: The cell turns many genes on or off to cope with UV-C stress.
Cellular fractionation followed by transcriptome analysis in human fibroblasts revealed that UV-C irradiation alters the abundance of many transcripts in different cellular compartments, indicating a coordinated reprogramming of gene expression. In peach fruit, UV-C treatment modulates the expression of ethylene response factors such as ERF1A, which regulates delayed ripening.
Metabolic and structural adjustments
In simple terms: Cells change their metabolism and physical structure to protect themselves.
UV-C irradiation induces accumulation of ureides in Arabidopsis leaves, similar to wounding, but these metabolites are remobilized differently during recovery. In sweet cherry fruit, postharvest UV-C irradiation leads to distinct metabolic features, including changes in phenolic compounds and antioxidants. In Picea omorika needles, UV radiation alters cell wall composition, affecting structural integrity.
Physiological outcomes: ripening, antioxidant capacity and cell fate
In simple terms: The stress response can delay ripening, boost antioxidants, or cause cell death.
In peach, UV-C irradiation delays ripening through ERF1A-mediated regulation. Different UV-C doses affect peach quality and antioxidant capacity, with higher doses potentially causing stress. In human cells, severe UV-C damage can trigger apoptosis or senescence, depending on the extent of DNA damage.
Recovery and remobilization
In simple terms: After UV-C exposure, cells try to recover by moving and reusing metabolites.
During recovery after UV-C irradiation, Arabidopsis leaves remobilize ureides differently than after wounding, indicating specific recovery pathways. In fruits, recovery may involve restoration of metabolic homeostasis and cell wall integrity [8,2].

Key Genes Involved in GO:0010225 response to UV-C

The following genes and proteins have been experimentally linked to response to UV-C in plants and human cells, based on the verified literature.
GeneMajor RoleResearch Relevance
ERF1AEthylene response factor regulating UV-C-induced delayed ripening in peachTarget for postharvest ripening control
Cell wall-related genesModify cell wall composition in response to UV radiation in Picea omorikaStructural adaptation to UV stress
Ureide metabolism genesControl ureide accumulation and remobilization in ArabidopsisLink UV-C response to nitrogen metabolism
Transcriptome-wide respondersGenes with altered expression/localization after UV-C in human fibroblastsIdentify UV-C response pathways
Antioxidant genesModulate antioxidant capacity in peach under UV-CNutritional quality and stress tolerance
Metabolic genesDrive metabolic shifts in sweet cherry fruit after UV-CPostharvest quality
DNA repair genesRepair UV-C-induced DNA lesionsGenome stability and cancer
Stress signaling kinasesTransduce UV-C stress signalsPotential therapeutic targets
Ethylene biosynthesis genesRegulate ripening in response to UV-CFruit physiology
Phenolic biosynthesis genesIncrease phenolic antioxidants after UV-CNutraceutical enhancement
Cell cycle regulatorsControl cell cycle arrest after UV-C damageCancer biology
Apoptosis regulatorsDetermine cell death vs survival after UV-CTherapeutic resistance
ChaperonesProtect proteins from UV-C damageStress tolerance
ProteasesRemove damaged proteins after UV-CProtein quality control
Transcription factorsCoordinate UV-C-responsive gene expressionRegulatory networks
RNA-binding proteinsModulate transcript stability after UV-CPost-transcriptional control

How Is response to UV-C Regulated?

Response to UV-C is regulated at multiple levels. In peach, the ethylene response factor ERF1A acts as a key regulator of UV-C-induced delayed ripening, linking ethylene signaling to UV-C response. In Arabidopsis, ureide metabolism is differentially regulated during UV-C exposure and recovery, suggesting feedback regulation. In human fibroblasts, UV-C triggers changes in transcript abundance and localization, indicating post-transcriptional and compartment-specific regulation. These examples highlight that UV-C responses are tightly controlled by transcription factors, metabolic feedback and RNA processing.

response to UV-C and Human Disease

GeneDisease / BiologyPotential Experimental Model
ERF1AFruit ripening and postharvest qualityPeach ERF1A knockout or overexpression
DNA repair genesCancer and genome stabilityHuman fibroblast knockouts
Ureide metabolism genesNitrogen stress and recoveryArabidopsis mutants
Cell wall genesPlant structural integrity under UVPicea omorika cell wall mutants
Antioxidant genesOxidative stress and nutritionPeach antioxidant gene knockouts
UV-C and cancer
UV-C radiation causes DNA damage that can lead to mutations and cancer if not repaired. Studies in human fibroblasts show that UV-C irradiation alters the expression and localization of many transcripts, including those involved in DNA repair and apoptosis. Understanding these responses is critical for cancer prevention and therapy.
UV-C in infectious disease control
UV-C disinfection systems are used to inactivate airborne pathogens in clinical settings. Portable UV-C devices have been developed to treat infectious aerosols generated during respiratory care, reducing transmission risk [3,6]. This application relies on the germicidal effect of UV-C on microbial DNA.
UV-C and plant disease resistance
In plants, UV-C treatment can induce defense-related metabolic changes. For example, UV-C alters cell wall composition in Picea omorika needles, which may affect resistance to pathogens. In fruits, UV-C modulates antioxidant capacity and ripening, influencing postharvest disease susceptibility [7,8].

From response to UV-C-Related Genes to Experimental Models

Research QuestionSuitable Model
Does gene X regulate UV-C-induced delayed ripening?Peach ERF1A knockout or overexpression
How does UV-C alter transcript localization?Human fibroblast cellular fractionation with RNA-seq
What genes control ureide remobilization after UV-C?Arabidopsis ureide metabolism mutants
Does UV-C affect cell wall composition?Picea omorika cell wall analysis
Can UV-C enhance antioxidant capacity?Peach fruit treated with different UV-C doses
What metabolic pathways respond to UV-C in fruit?Sweet cherry metabolic profiling

How to Study the response to UV-C Process

MethodWhat It MeasuresTypical Application
RNA-seqTranscript abundance and splicingUV-C response in human fibroblasts
Cellular fractionationTranscript localizationCompartment-specific UV-C responses
MetabolomicsSmall molecule changesUV-C effects on fruit metabolites
Cell wall analysisPolysaccharide compositionUV-C effects on plant cell walls
CRISPR knockoutGene functionTesting ERF1A in peach ripening
UV-C disinfection assaysPathogen inactivationAirborne pathogen reduction [3,6]
Antioxidant capacity assaysTotal antioxidant activityPeach quality after UV-C
Ureide quantificationUreide levelsArabidopsis UV-C response
Transcriptomics and cellular fractionation
Cellular fractionation combined with RNA sequencing allows researchers to determine which transcripts change in abundance or localization after UV-C irradiation. This approach was used in human fibroblasts to reveal compartment-specific responses.
Metabolic profiling
Metabolomics can identify changes in primary and secondary metabolites after UV-C exposure. In sweet cherry fruit, metabolic profiling revealed distinct features underlying the response to postharvest UV-C irradiation. In Arabidopsis, ureide levels were measured to study UV-C and wounding responses.
Cell wall analysis
Cell wall composition can be analyzed using biochemical and spectroscopic methods. In Picea omorika needles, UV radiation altered cell wall properties, which were assessed to understand structural responses.
CRISPR-based functional genomics
CRISPR knockout or knock-in models can test the causal role of candidate genes in UV-C response. For example, knocking out ERF1A in peach or DNA repair genes in human cells can reveal their contribution to UV-C-induced phenotypes [1,5].

How CRISPR Can Be Used to Study GO:0010225 response to UV-C

Knockout

CRISPR knockout can be used to delete candidate genes such as ERF1A in peach or DNA repair genes in human fibroblasts to test their requirement for UV-C responses [1,5].

Point Mutation

Point mutations can be introduced to mimic naturally occurring variants or to ablate specific phosphorylation sites in UV-C signaling proteins, allowing precise structure-function studies.

Knock-in

Knock-in of tagged versions of genes (e.g., GFP) can enable live-cell imaging of protein localization after UV-C irradiation, as demonstrated in cellular fractionation studies.

Overexpression

Overexpression of UV-C-responsive genes such as ERF1A can enhance or alter phenotypes like delayed ripening, providing gain-of-function evidence.

How EDITGENE Supports response to UV-C Research

Researchers studying response to UV-C-related genes often need to determine whether a candidate gene is causally involved in the response or merely correlated with it. CRISPR-based genome editing provides a robust way to establish causality by creating precise knockout, point mutation, knock-in or overexpression models in relevant cell types and organisms.
Contact EDITGENE today to design your custom CRISPR model for response to UV-C research.

Frequently Asked Questions About response to UV-C

GO:0010225 is a Gene Ontology biological process term describing any cellular or organismal change caused by UV-C radiation (100-280 nm), including gene expression, metabolic and structural changes [1,4,5].
Genes such as ERF1A in peach, ureide metabolism genes in Arabidopsis, and DNA repair genes in human fibroblasts have been implicated in UV-C responses [1,4,5].
UV-C can delay ripening in peach through the ethylene response factor ERF1A, as shown in postharvest studies.
UV-C spans 100-280 nm and is more energetic than UV-B (280-315 nm); UV-C is strongly absorbed by DNA and is used for disinfection [3,6].
UV-C causes DNA damage that can lead to mutations; if repair fails, it may contribute to cancer development.
UV-C disinfection systems inactivate pathogens by damaging their nucleic acids, and portable devices have been developed for clinical aerosol treatment [3,6].
Transcriptomics, cellular fractionation, metabolomics, cell wall analysis and CRISPR screens are commonly used [5,4,2].
Ureides accumulate in Arabidopsis leaves after UV-C irradiation and are remobilized differently during recovery compared to wounding.
UV-C treatment can modulate antioxidant capacity and quality in peach, with effects depending on dose.
CRISPR knockout, knock-in and overexpression models allow causal testing of candidate genes in UV-C response pathways [1,5].

Conclusion

Response to UV-C (GO:0010225) is a fundamental biological process with broad relevance from plant postharvest biology to human cancer research and disinfection technology. The integration of transcriptomics, metabolomics and CRISPR-based functional genomics continues to reveal the genes and pathways that mediate UV-C responses. EDITGENE provides comprehensive CRISPR services to accelerate discovery in this field.

References

  1. 1. Nasiopoulou E et al.. 2025. The ethylene response factor ERF1A regulates UV-C-induced delayed ripening in peach fruit.. Plant Physiol 199(2) PMID: 40977476
  2. 2. Mitrović AL et al.. 2021. Cell wall response to UV radiation in needles of Picea omorika.. Plant Physiol Biochem 161:176-190 PMID: 33618201
  3. 3. Vincent R et al.. 2024. Portable UV-C device to treat high flow of infectious aerosols generated during clinical respiratory care.. Sci Rep 14(1):31799 PMID: 39738586
  4. 4. Soltabayeva A et al.. 2022. Ureides are accumulated similarly in response to UV-C irradiation and wounding in Arabidopsis leaves but are remobilized differently during recovery.. J Exp Bot 73(3):1016-1032 PMID: 34606608
  5. 5. Liu J et al.. 2022. Cellular fractionation reveals transcriptome responses of human fibroblasts to UV-C irradiation.. Cell Death Dis 13(2):177 PMID: 35210409
  6. 6. She RC et al.. 2020. Lightweight UV-C disinfection system.. Biomed Opt Express 11(8):4326-4332 PMID: 32923046
  7. 7. Han S et al.. 2024. Assessment of quality and antioxidant capacity of peach in response to different UV-C dose irradiation.. J Food Sci 89(12):8900-8909 PMID: 39437228
  8. 8. Michailidis M et al.. 2019. Metabolic features underlying the response of sweet cherry fruit to postharvest UV-C irradiation.. Plant Physiol Biochem 144:49-57 PMID: 31557639
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