GO:0071494 cellular response to UV-C: DNA Damage Response, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0071494 cellular response to UV-C describes all cellular changes triggered by shortwave ultraviolet radiation (100-280 nm), including transcriptional reprogramming, DNA repair, oxidative stress responses and cell wall remodeling [1, 4, 5].
• UV-C is strongly absorbed by nucleic acids and proteins, making it a potent genotoxic and germicidal agent that activates complex survival and death pathways.
• Transcriptomic studies in human fibroblasts show that UV-C rapidly alters the expression of hundreds of genes, with distinct nuclear and cytoplasmic responses.
• Non-mammalian models such as Dictyostelium discoideum, Pseudomonas aeruginosa, peach fruit and Picea omorika have revealed conserved and kingdom-specific UV-C response mechanisms [2, 3, 4, 5].
• Key protein players include poly(ADP-ribose) polymerase (PARP), topoisomerase I, ascorbate peroxidase, and ethylene response factors, which modulate DNA repair, redox balance and developmental arrest [2, 4, 7].
• CRISPR-based knockout, knock-in and overexpression models are essential to dissect causal roles of specific genes in the UV-C response and to identify therapeutic targets for UV-related skin damage and cancer [6, 8].
Description
The cellular response to UV-C (GO:0071494) is a biological process that encompasses all molecular and physiological changes occurring in a cell after exposure to ultraviolet C radiation (100-280 nm). UV-C is the shortest and most energetic UV wavelength that reaches the Earth's surface only from artificial sources such as germicidal lamps, but it is widely used experimentally to induce DNA damage and study stress responses. Because UV-C is strongly absorbed by DNA, RNA and proteins, it triggers a complex network of signaling events that determine cell fate, including DNA repair, cell cycle arrest, apoptosis and metabolic reprogramming [1, 8]. Understanding this process is critical for photobiology, cancer research, and the development of UV-protective strategies. Recent transcriptomic profiling of human fibroblasts has revealed that UV-C irradiation causes rapid and extensive changes in gene expression, with distinct responses in nuclear and cytoplasmic fractions. Beyond mammalian cells, UV-C responses have been characterized in diverse organisms such as the social amoeba Dictyostelium discoideum, the bacterium Pseudomonas aeruginosa, peach fruit and Serbian spruce, highlighting both conserved and specialized adaptation mechanisms [2, 3, 4, 5]. This article integrates authoritative QuickGO annotation with verified PubMed literature to provide a research-grade overview of GO:0071494, its key genes, regulatory mechanisms, disease relevance and experimental models.
cellular response to UV-C At A Glance
| GO ID | GO:0071494 |
|---|---|
| GO term | cellular response to UV-C |
| Ontology | biological_process |
| Synonym | cellular response to germicidal ultraviolet light stimulus; cellular response to shortwave ultraviolet radiation stimulus; cellular response to UV-C light stimulus; cellular response to UVC radiation stimulus |
| Major function | Coordinated cellular defense against UV-C-induced damage, including DNA repair, oxidative stress response, transcriptional reprogramming and cell fate decisions |
| Taxonomic range | Observed in bacteria, protists, plants, fungi and animals, indicating broad evolutionary conservation |
| Key molecular triggers | DNA photoproducts (cyclobutane pyrimidine dimers, 6-4 photoproducts), reactive oxygen species, protein damage |
| Experimental models | Human fibroblasts, mouse ocular surface cells, Dictyostelium discoideum, Pseudomonas aeruginosa, peach fruit, Picea omorika |
| Related GO terms | cellular response to UV, response to UV-C, DNA repair, apoptotic process |
What Is GO:0071494?
According to the Gene Ontology, GO:0071494 cellular response to UV-C is defined as any process that results in a change in state or activity of a cell (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a UV-C radiation stimulus. UV-C radiation spans wavelengths from 100 to 280 nm. This term covers the cellular reception of UV-C photons, signal transduction, and the downstream effector responses that collectively determine cell survival, adaptation or death.
Why Is cellular response to UV-C Important in Cell Biology?
GO:0071494 is important because UV-C radiation is a powerful tool for studying fundamental DNA damage responses and because it is increasingly used in germicidal applications, food preservation and cancer therapy. The cellular response to UV-C determines whether a cell repairs damage and survives or undergoes apoptosis, and dysregulation of these pathways contributes to skin cancer, premature aging and inflammatory diseases. Moreover, understanding UV-C responses in non-mammalian organisms informs biotechnology and agricultural applications, such as delaying fruit ripening or controlling bacterial contamination [2, 3].
• UV-C is a major environmental and artificial genotoxic agent that directly damages DNA, making its cellular response central to mutagenesis and carcinogenesis research.
• The response to UV-C involves complex transcriptional programs that can be harnessed to identify biomarkers of UV exposure and DNA repair capacity.
• Defects in UV-C response pathways are linked to xeroderma pigmentosum and other photosensitive disorders, highlighting clinical relevance.
• UV-C-based germicidal technologies require understanding of microbial UV-C responses to optimize inactivation and prevent resistance.
• In plants, UV-C responses influence secondary metabolism, cell wall integrity and postharvest quality, with agricultural implications [2, 5].
• Model organisms like Dictyostelium discoideum provide tractable systems to dissect evolutionarily conserved DNA damage responses.
• UV-C response studies inform the development of radioprotective compounds and antioxidants for ocular and skin protection [6, 7].
• CRISPR screens targeting UV-C response genes can uncover novel therapeutic targets for cancer and degenerative diseases [1, 8].
What Happens During cellular response to UV-C?
Photon absorption and primary damage
In simple terms: UV-C light hits the cell and directly damages DNA and other molecules.
UV-C photons (100-280 nm) are absorbed by nucleic acids and proteins, leading to the formation of cyclobutane pyrimidine dimers and 6-4 photoproducts in DNA, as well as oxidative damage through reactive oxygen species generation. In human fibroblasts, this primary damage triggers rapid changes in the transcriptome, with distinct gene expression signatures in nuclear and cytoplasmic compartments. In bacteria such as Pseudomonas aeruginosa, UV-C exposure activates the Alp and Prt regulons, which are involved in stress response and virulence.
DNA damage recognition and repair
In simple terms: The cell detects broken DNA and tries to fix it.
Following UV-C-induced DNA damage, cells activate nucleotide excision repair (NER) and other repair pathways. Poly(ADP-ribose) polymerase (PARP) is rapidly recruited to damage sites and synthesizes poly(ADP-ribose) chains to facilitate repair; in Dictyostelium discoideum, PARP activity is essential for surviving UV-C stress. Topoisomerase I deficiency in carrot cells leads to increased sensitivity to UV-C, indicating a role for topoisomerase I in maintaining genome stability under UV-C stress.
Transcriptional reprogramming
In simple terms: The cell changes which genes are turned on or off to cope with the damage.
UV-C irradiation induces widespread changes in gene expression. In human fibroblasts, cellular fractionation followed by RNA sequencing revealed that UV-C alters the transcriptome in both nuclear and cytoplasmic fractions, affecting genes involved in DNA repair, apoptosis, cell cycle and RNA processing. In peach fruit, the ethylene response factor ERF1A regulates UV-C-induced delayed ripening, demonstrating that UV-C can modulate developmental programs through specific transcription factors.
Oxidative stress and antioxidant response
In simple terms: UV-C creates harmful oxygen molecules, and the cell boosts its defenses.
UV-C exposure generates reactive oxygen species (ROS) that can damage lipids, proteins and DNA. In primary mouse ocular surface cells, UV-C induces oxidative damage that can be assessed by markers of lipid peroxidation and DNA oxidation. Carrot cells with low ascorbate levels show increased sensitivity to UV-C, and ascorbate peroxidase activity is important for detoxifying ROS. In Picea omorika needles, UV radiation triggers cell wall remodeling as part of the oxidative stress response.
Cell fate decisions: survival, arrest or death
In simple terms: Depending on the damage, the cell may repair itself, stop dividing, or self-destruct.
The integration of DNA repair, oxidative stress and transcriptional signals determines cell fate. Severe UV-C damage can trigger apoptosis, while milder damage leads to cell cycle arrest and repair. In human fibroblasts, UV-C-induced transcriptome changes include pro-apoptotic and anti-apoptotic genes, reflecting a balance between survival and death. In Pseudomonas aeruginosa, UV-C exposure activates regulons that can lead to either adaptation or cell death depending on the dose and genetic background.
Key Genes Involved in GO:0071494 cellular response to UV-C
The following genes and proteins have been experimentally implicated in the cellular response to UV-C across various model systems.
| Gene | Major Role | Research Relevance |
|---|---|---|
| PARP1 | Poly(ADP-ribose) polymerase; DNA damage detection and repair | Essential for survival after UV-C in Dictyostelium; target for cancer therapy |
| TOP1 | Topoisomerase I; DNA relaxation and repair | Deficiency increases UV-C sensitivity in carrot cells |
| ERF1A | Ethylene response factor; transcriptional regulation | Regulates UV-C-induced delayed ripening in peach fruit |
| Alp regulon | Stress response and virulence genes in Pseudomonas | Activated by UV-C; potential antibacterial target |
| Prt regulon | Protease production and stress response | UV-C-induced in Pseudomonas aeruginosa |
| APX | Ascorbate peroxidase; ROS detoxification | Low ascorbate levels increase UV-C sensitivity in carrot |
| XPA | DNA damage recognition in nucleotide excision repair | Defects cause xeroderma pigmentosum; UV-C hypersensitivity |
| XPC | DNA damage recognition in global genome NER | Mutations linked to skin cancer predisposition |
| TP53 | Tumor suppressor; cell cycle arrest and apoptosis | Central to UV-C-induced cell fate decisions |
| CDKN1A | p21; cell cycle inhibitor | Induced by UV-C to allow DNA repair |
| GADD45A | Growth arrest and DNA damage-inducible | Upregulated after UV-C; involved in repair |
| MDM2 | p53 regulator; apoptosis modulation | UV-C-induced transcriptome changes include MDM2 |
| BAX | Pro-apoptotic Bcl-2 family member | Mediates UV-C-induced apoptosis |
| BCL2 | Anti-apoptotic protein | Modulates survival after UV-C |
| PCNA | Proliferating cell nuclear antigen; DNA replication and repair | Required for post-UV-C repair synthesis |
| RAD51 | Homologous recombination repair | Contributes to UV-C damage repair |
| OGG1 | 8-oxoguanine DNA glycosylase; base excision repair | Repairs oxidative DNA damage from UV-C |
| NFE2L2 | Nrf2; antioxidant response transcription factor | Regulates antioxidant genes after UV-C |
How Is cellular response to UV-C Regulated?
The cellular response to UV-C is regulated at multiple levels. Transcriptional regulation involves stress-responsive transcription factors such as p53, NF-kB and Nrf2, which coordinate the expression of DNA repair, antioxidant and apoptotic genes [1, 8]. Post-translational modifications, including phosphorylation by ATM/ATR kinases, ubiquitination and poly(ADP-ribosyl)ation, rapidly modulate protein activity and stability [4, 8]. In plants, ethylene signaling through ERF1A regulates UV-C-induced developmental changes. In bacteria, two-component systems and alternative sigma factors control the Alp and Prt regulons in response to UV-C. Additionally, microRNAs and RNA-binding proteins contribute to post-transcriptional regulation of UV-C response genes.
cellular response to UV-C and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| XPA | Xeroderma pigmentosum; UV hypersensitivity | Knockout in human fibroblasts or keratinocytes |
| TP53 | Skin cancer; Li-Fraumeni syndrome | Point mutation knock-in in mouse models |
| PARP1 | Cancer susceptibility; DNA repair deficiency | Knockout in Dictyostelium or human cell lines |
| OGG1 | Oxidative DNA damage; cancer risk | Knockout in mouse ocular surface cells |
| ERF1A | Fruit ripening regulation | Overexpression or knockout in peach fruit |
UV-C response defects and skin cancer
Inherited defects in nucleotide excision repair, such as xeroderma pigmentosum, cause extreme sensitivity to UV radiation and a dramatically increased risk of skin cancer. The cellular response to UV-C is critical for removing UV-induced DNA lesions; failure to do so leads to mutations in genes like TP53 and subsequent carcinogenesis. Studying UV-C responses in human fibroblasts helps identify biomarkers of DNA repair capacity and targets for chemoprevention.
Ocular surface damage and oxidative stress
The ocular surface is constantly exposed to UV radiation, and UV-C can induce oxidative damage in corneal and conjunctival cells. Primary mouse ocular surface cells show increased oxidative stress markers after UV-C exposure, and antioxidant defenses are crucial for protection. Understanding these responses can inform the development of protective eye drops or treatments for UV-related ocular surface diseases.
Microbial UV-C resistance and infection control
Pseudomonas aeruginosa responds to UV-C by activating the Alp and Prt regulons, which may contribute to survival and virulence. Understanding these regulatory networks can help optimize UV-C disinfection protocols and prevent the emergence of resistant strains in clinical settings.
Plant UV-C responses and agricultural quality
In peach fruit, UV-C treatment delays ripening through the action of ERF1A, offering a postharvest technology to extend shelf life. In Picea omorika, UV-C triggers cell wall changes that may affect stress tolerance. These findings link UV-C response pathways to crop quality and forest health.
From cellular response to UV-C-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does gene X protect against UV-C-induced apoptosis? | CRISPR knockout in human fibroblasts followed by UV-C and viability assay |
| What is the role of a specific point mutation in DNA repair? | Knock-in of point mutation in endogenous locus using CRISPR |
| How does a gene affect UV-C-induced transcriptional changes? | Knockout or overexpression combined with RNA-seq |
| Can a candidate gene rescue UV-C sensitivity in a deficient background? | Overexpression in knockout cells |
| What is the subcellular localization of a protein after UV-C? | Tagged knock-in with fluorescent protein |
| Which genes are essential for UV-C survival in bacteria? | CRISPR interference library screening in Pseudomonas |
How to Study the cellular response to UV-C Process
| Method | What It Measures | Typical Application |
|---|---|---|
| RNA-seq | Global gene expression changes | Transcriptome profiling after UV-C |
| Comet assay | DNA strand breaks and repair | Quantifying UV-C-induced DNA damage |
| gamma-H2AX immunofluorescence | DNA double-strand breaks and repair foci | Assessing repair protein recruitment |
| ROS detection (DCFDA, MitoSOX) | Reactive oxygen species levels | Oxidative stress measurement |
| CRISPR knockout screen | Gene essentiality and fitness under UV-C | Discovery of novel UV-C response genes |
| Western blot | Protein expression and modification | Validating candidate gene expression |
| qRT-PCR | Specific gene expression | Confirming RNA-seq findings |
| Cell viability assay (MTT, ATP) | Cell survival after UV-C | Evaluating protective or sensitizing interventions |
Transcriptomics and RNA sequencing
RNA-seq is widely used to profile global gene expression changes after UV-C irradiation. Cellular fractionation followed by RNA-seq can distinguish nuclear and cytoplasmic transcript pools, revealing post-transcriptional regulation. This method identifies differentially expressed genes, pathways and potential biomarkers of UV-C exposure.
DNA damage and repair assays
Comet assay, immunofluorescence for gamma-H2AX and measurement of cyclobutane pyrimidine dimers are standard methods to quantify UV-C-induced DNA damage and repair kinetics. These assays can be combined with gene knockout or overexpression to assess the role of specific factors.
Oxidative stress measurements
Reactive oxygen species (ROS) levels, lipid peroxidation and antioxidant enzyme activities can be measured using fluorescent probes, colorimetric assays and enzyme activity kits. In ocular surface cells, oxidative damage markers are assessed after UV-C exposure. In plant cells, ascorbate peroxidase activity is a key indicator.
CRISPR screening and functional genomics
Pooled CRISPR knockout or activation screens can identify genes that modulate UV-C sensitivity or resistance. Such screens are particularly powerful in human cell lines and bacteria, enabling unbiased discovery of novel UV-C response regulators [1, 3].
How CRISPR Can Be Used to Study GO:0071494 cellular response to UV-C
Knockout
CRISPR knockout is used to delete candidate genes and assess their requirement for UV-C survival, DNA repair or transcriptional responses. For example, knocking out PARP1 in Dictyostelium discoideum increases UV-C sensitivity, demonstrating its essential role. In human cells, knockout of XPA or XPC leads to defective nucleotide excision repair and hypersensitivity to UV-C.
Point Mutation
Point mutation knock-in allows precise modeling of disease-associated variants or functional residues. For instance, introducing a catalytically dead mutation in PARP1 or a phosphorylation site mutation in p53 can reveal specific domains required for UV-C response [4, 8]. This approach is valuable for dissecting signaling mechanisms.
Knock-in
Knock-in of reporter genes or tags (e.g., GFP, luciferase) enables real-time monitoring of protein localization, stability and interactions after UV-C. Tagged knock-in of DNA repair proteins can visualize their recruitment to damage sites. Knock-in of a resistance allele can also test sufficiency in a knockout background.
Overexpression
Overexpression of wild-type or mutant genes is used to test gain-of-function effects on UV-C sensitivity. For example, overexpressing antioxidant enzymes like ascorbate peroxidase can protect carrot cells from UV-C-induced oxidative damage. In peach fruit, overexpression of ERF1A alters ripening delay.
How EDITGENE Supports cellular response to UV-C Research
Researchers studying cellular response to UV-C-related genes often need to determine whether a candidate gene is causally involved in DNA repair, oxidative stress or cell fate decisions. EDITGENE provides comprehensive CRISPR-based services to generate precisely engineered cell models, enabling rigorous functional validation and drug discovery.
Contact EDITGENE today to design your custom CRISPR model for cellular response to UV-C research.
Frequently Asked Questions About cellular response to UV-C
What is GO:0071494 cellular response to UV-C?
GO:0071494 is a Gene Ontology biological process term that describes all changes in a cell's state or activity caused by UV-C radiation (100-280 nm), including DNA repair, gene expression changes and oxidative stress responses [1, 8].
What genes are involved in the cellular response to UV-C?
Key genes include PARP1, TOP1, ERF1A, XPA, XPC, TP53, CDKN1A, GADD45A, BAX, BCL2, PCNA, RAD51, OGG1 and NFE2L2, as identified in various model organisms [1, 2, 4, 7, 8].
How does UV-C damage cells?
UV-C is absorbed by DNA and proteins, causing cyclobutane pyrimidine dimers, 6-4 photoproducts and reactive oxygen species that damage lipids, proteins and DNA.
What is the difference between UV-C and UV-B?
UV-C spans 100-280 nm and is more energetic than UV-B (280-315 nm); UV-C is mostly absorbed by the ozone layer and is used artificially for germicidal purposes, while UV-B reaches the Earth's surface and causes sunburn.
Which model organisms are used to study UV-C response?
Common models include human fibroblasts, mouse ocular surface cells, Dictyostelium discoideum, Pseudomonas aeruginosa, peach fruit and Picea omorika [1, 2, 3, 4, 5, 6].
How can CRISPR be used to study UV-C response genes?
CRISPR knockout, knock-in, point mutation and overexpression can be used to test the causal role of specific genes in UV-C survival, DNA repair and transcriptional responses [1, 4, 8].
What are the main signaling pathways in UV-C response?
Key pathways include nucleotide excision repair, p53-mediated apoptosis and cell cycle arrest, PARP-dependent DNA damage signaling, and Nrf2-mediated antioxidant response [1, 4, 8].
Does UV-C cause cancer?
UV-C is a known carcinogen in experimental models, but its role in human cancer is limited because it is filtered by the atmosphere. However, studying UV-C responses helps understand UV-B and UV-A carcinogenesis.
What methods are used to measure UV-C response?
Methods include RNA-seq, comet assay, gamma-H2AX immunofluorescence, ROS detection, CRISPR screens, western blot and cell viability assays [1, 6, 8].
How does UV-C affect plant cells?
In plants, UV-C triggers cell wall remodeling, oxidative stress responses and delayed ripening through transcription factors like ERF1A [2, 5].
Conclusion
GO:0071494 cellular response to UV-C is a fundamental biological process that integrates DNA damage detection, transcriptional reprogramming, oxidative stress management and cell fate decisions. Research across diverse organisms has revealed conserved and specialized mechanisms, with key roles for PARP1, topoisomerase I, p53 and antioxidant enzymes. Understanding these pathways has broad implications for cancer biology, photoprotection, microbial disinfection and agricultural biotechnology. CRISPR-based models and functional genomics are powerful tools to dissect the causal roles of individual genes and to identify new therapeutic targets. EDITGENE provides end-to-end CRISPR services to accelerate this research.
References
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- 3. Fonseca MRB et al.. 2026. Roles of Alp and Prt Regulons in the Response of Pseudomonas aeruginosa to UV-C Light.. Environ Microbiol Rep 18(1):e70268 PMID: 41527391
- 4. Mir H et al.. 2015. Response of Dictyostelium discoideum to UV-C and involvement of poly (ADP-ribose) polymerase.. Cell Prolif 48(3):363-74 PMID: 25858552
- 5. Mitrović AL et al.. 2021. Cell wall response to UV radiation in needles of Picea omorika.. Plant Physiol Biochem 161:176-190 PMID: 33618201
- 6. Bose B et al.. 2020. Assessment of Oxidative Damage in the Primary Mouse Ocular Surface Cells/Stem Cells in Response to Ultraviolet-C (UV-C) Damage.. J Vis Exp PMID: 32116303
- 7. Balestrazzi A et al.. 2010. Response to UV-C radiation in topo I-deficient carrot cells with low ascorbate levels.. J Exp Bot 61(2):575-85 PMID: 19917599
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