UV radiation tolerant
traitmech:000009 · CLASS · REVIEWED
An environmental tolerance in which an organism survives high doses of ultraviolet radiation, typically via photoreactivation and nucleotide-excision repair of cyclobutane pyrimidine dimers and 6-4 photoproducts.
UV-radiation tolerance via nucleotide-excision and photoreactivation repair
Edge evidence
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ultraviolet radiation
challenges
UV radiation tolerant
METPO:2007406UV exposure is the environmental challenge the trait counters.
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DOI:10.3390/genes14091803
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nucleotide-excision repair
confers
UV radiation tolerant
METPO:2007700NER removes UV-induced cyclobutane pyrimidine dimers and 6-4 photoproducts.
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DOI:10.3390/genes14091803
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photoreactivation
confers
UV radiation tolerant
METPO:2007700Photolyase-mediated dimer reversal complements excision repair.
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DOI:10.1101/cshperspect.a012765
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ultraviolet radiation
causes
cyclobutane pyrimidine dimer
biolink:causesUV exposure produces cyclobutane pyrimidine dimers, the majority DNA lesion.
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DOI:10.3390/life14070822
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ultraviolet radiation
causes
pyrimidine (6-4) pyrimidone photoproduct
biolink:causesUV exposure produces pyrimidine (6-4) pyrimidone photoproducts.
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DOI:10.3390/life14070822
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CPD photolyase
repairs
cyclobutane pyrimidine dimer
CPD photolyase directly reverses cyclobutane pyrimidine dimers via light-driven electron transfer.
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DOI:10.3390/ijms241512381
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catalase
detoxifies
reactive oxygen species
Catalase scavenges UV-induced reactive oxygen species, preventing oxidative damage.
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DOI:10.3390/microorganisms13040756
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mycosporine-like amino acids
absorbs
ultraviolet radiation
MAAs absorb UV-A/UV-B (~309-362 nm) and release it as harmless heat, screening UV.
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DOI:10.3390/ijms241512381
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mycosporine-like amino acids
quenches
reactive oxygen species
MAAs act as antioxidants that quench UV-induced reactive oxygen species.
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DOI:10.3390/ijms241512381
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Provenance
- Source
- METPO (2025-11-25)
- Definition source
- DOI:10.3390/genes14091803
Parent traits (1)
Synonyms (1)
- UV resistant
kg-microbe context
Matched 1 kg-microbe node via parent_proxy.
METPO:1000059[-2.682, -2.070, -3.656, -0.652, …]
Nearest neighbors in embedding space
- environment cadmium tolerant 1.000
- morphology sulfur globule 1.000
- environment cobalt tolerant 1.000
- environment copper tolerant 1.000
- environment desiccation tolerant 1.000
- environment piezotolerant 1.000
- environment obligately piezophilic 1.000
- morphology gas vesicle 1.000
Deep research
# Curation report: microbial UV-radiation tolerance ## Trait record and recommendation - **Trait label:** UV radiation tolerant - **Trait identifier:** `traitmech:000009` - **Category / term kind / status:** ENVIRONMENT / CLASS / REVIEWED - **Parent:** `traitmech:000007` - **Synonym:** UV resistant **Recommended scope.** This trait should denote a reproducible capacity of a microorganism to retain viability or reproductive capacity after a defined ultraviolet exposure. A valid phenotype record should specify wavelength or band, fluence in J m⁻², dose rate where known, physiological state, medium, shielding conditions, and whether recovery occurred in photoreactivating light or darkness. These variables are mechanistically decisive: haloarchaeal survival was measured at 254-nm UV-C and 0–144 J m⁻² under light versus dark recovery, whereas a *Pseudomonas syringae* study used solar UV-B at 4.5 kJ m⁻² over 290–320 nm. The resulting values are not directly interchangeable. (gunasekera2006roleofnucleotide pages 1-2, nag2023genomicanalysisof pages 2-4) The supplied definition is substantially correct but too narrow if interpreted as universal. Photoreactivation and nucleotide-excision repair (NER) are the best-supported core mechanisms, but auxiliary recombinational, DNA-end-protection, antioxidant, pigment, sporulation, biofilm, and physical-shielding mechanisms can contribute in particular taxa or assays. The graph should therefore represent photoreactivation and NER as the conserved core while placing *Deinococcus*-specific and lineage-specific systems in qualified extensions. ## 1. Trait scope and boundary cases ### Included phenotype A strain is UV-radiation tolerant when its survival curve, D-value, surviving fraction at a specified fluence, or post-exposure growth is substantially greater than an appropriate comparator under the same conditions. For example, *Deinococcus radiodurans* survives doses up to approximately 750 J m⁻² in the cited experiment, compared with about 30 J m⁻² for *E. coli* B/r; 500 J m⁻² generated approximately 5,000 thymine-containing pyrimidine dimers per *D. radiodurans* genome, or about one lesion per 640 bp. (selvam2013ddraddrdand pages 1-2) The phenotype may include: 1. **Intrinsic damage prevention**, such as molecular absorption or quenching, when experimentally linked to cellular survival. 2. **Direct reversal**, principally visible-light-dependent photoreactivation. 3. **Damage excision and resynthesis**, principally UvrABC-dependent NER. 4. **Damage tolerance and genome restoration**, including recombination, stress regulation, and taxon-specific DNA-protection proteins. 5. **Community- or structure-mediated protection**, such as spores, aggregates, extracellular matrix, or pigments, but only when the curated subject is explicitly the corresponding structured state rather than an unshielded vegetative cell. ### Exclusions and nearby traits - **Ionizing-radiation resistance is not equivalent.** Gamma/X-ray resistance involves extensive oxidative damage and double-strand breaks; overlap with UV tolerance does not justify transferring a gamma-radiation D10 value into this trait. - **Desiccation tolerance is distinct.** Shared protein-protection and DNA-repair systems may create correlated phenotypes, especially in *Deinococcus*, but desiccation survival is not evidence of UV survival by itself. - **UV avoidance is not cellular tolerance.** Burial, motility away from light, host-tissue protection, mineral shielding, and self-shading reduce received dose. Curate these as exposure modifiers unless survival of directly irradiated cells is demonstrated. - **Inactivation is not necessarily death.** Loss of colony formation, membrane damage, delayed growth, and inability to infect are different endpoints. - **Gene presence is not phenotype evidence.** A predicted photolyase, NER operon, pigment cluster, or antioxidant gene supports mechanistic potential, not the trait, without a survival assay or functional perturbation. - **Photoreactivation must be separated from dark repair.** Light after exposure can strongly increase apparent resistance; studies that do not control post-irradiation illumination may conflate damage induction with recovery capacity. ## 2. Current mechanistic model UV-B and UV-C induce bulky DNA photolesions, especially cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproducts. These lesions impede replication and transcription and may produce mutagenesis or loss of viability. In the best-supported graph, lesion removal branches into two routes: 1. **Photoreactivation:** lesion-specific photolyases bind CPDs or 6-4 photoproducts and use photoreactivating light to reverse the lesion. 2. **Dark repair:** UvrA/UvrB recognize damaged DNA, UvrC incises it, and downstream excision, synthesis, and ligation restore the duplex. The routes can be strongly complementary. In *P. syringae*, either a `phr` or `uvrA` mutation reduced survival by approximately 10²-fold, whereas the double mutant was reduced by more than 10⁶-fold under solar UV-B. The same study observed a faster and stronger RecA-mediated SOS response in repair mutants, consistent with accumulation of unrepaired lesions; this supports an edge from damage accumulation to SOS induction, but not by itself a direct edge from SOS induction to tolerance. (gunasekera2006roleofnucleotide pages 1-2) In marine *Synechococcus* RS9916, photoreactivation accounted for most recovery, and multiple photolyases collectively supported exceptional survival. At 1,000 J m⁻² UV-B and 250 J m⁻² UV-C, survival differences relative to *E. coli* were reported on the order of one million-fold and 100,000-fold, respectively. However, assignments of Phr2/Phr3 as CPD photolyases and Phr4/Phr5 as a 6-4 photolyase remain sequence/structure-based predictions pending direct biochemical substrate assays. (haney2022multiplephotolyasesprotect pages 12-13, haney2022multiplephotolyasesprotect pages 4-7) ## 3. Candidate nodes ### Environmental and assay nodes | Candidate node | Type | Suggested grounding | Curation note | |---|---|---|---| | ultraviolet radiation | Environmental factor | **ENVO term to be resolved**; label-only until verified | Record UV-A, UV-B, or UV-C as assay qualifiers rather than treating them as equivalent. | | UV-B radiation | Experimental/environmental factor | Label-only candidate | Solar study: 290–320 nm, 4.5 kJ m⁻². (gunasekera2006roleofnucleotide pages 1-2) | | UV-C radiation | Experimental factor | Label-only candidate | Haloarchaeal study: 254 nm, 0–144 J m⁻². (nag2023genomicanalysisof pages 2-4) | | UV fluence | Measurement/assay attribute | Unit: J m⁻² | Mandatory quantitative qualifier when available. | | photoreactivating light | Experimental factor | Label-only candidate | Enables photolyase-dependent recovery; spectrum and duration should be recorded. | | dark recovery | Experimental condition | Label-only candidate | Operationally separates light-independent repair from photoreactivation. |
Curation history
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PROPOSED_FROM_RESEARCH · claude
Proposed candidate ENVIRONMENT trait (ultraviolet radiation tolerance) from literature research; sub-variant of radiotolerant.
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CURATED_CAUSAL_GRAPH · claude
Added evidence-backed causal graph (NER + photoreactivation) with GO node grounding and RO/METPO predicate groundings; promoted PROPOSED to REVIEWED.
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GROUND_CAUSAL_NODES · claude
Grounded 1 causal-node grounding field(s) via mappings/node_grounding.tsv (ENVO:21001216×1).
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ENRICH_CAUSAL_GRAPH · claude
Added 6 evidence-backed generic edges (6 new nodes) from the deep-research report.
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GROUND_CAUSAL_PREDICATES · claude
Grounded 2 causal-edge predicate_id field(s) via mappings/predicate_grounding.tsv (biolink:causes×2).
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GROUND_CAUSAL_NODES · claude
Grounded 1 causal-node grounding field(s) via mappings/node_grounding.tsv (UniProtKB:A0A071MK53×1).
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GROUND_CAUSAL_NODES · claude
Grounded 2 causal-node grounding field(s) via mappings/node_grounding.tsv (CHEBI:26523×1, CHEBI:35738×1).
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RETRACT_DEAD_UNIPROT_GROUNDINGS · claude
Retracted 1 UniProtKB grounding(s) whose accessions are deleted from UniProt; nodes demoted to label-only pending re-grounding (docs/GROUNDING_POLICY.md)
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GROUND_CAUSAL_NODES · claude
Grounded 1 causal-node grounding field(s) via mappings/node_grounding.tsv (GO:0004096×1).
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MIGRATE_ENABLES_TRAIT_EDGES · claude
Migrated 2 causal edge(s) off enables/RO:0002327 with a TRAIT object (2 to confers), issue 302. RO:0002327 has range 'biological process or activity', which a trait (a disposition) cannot satisfy, so the previous form entailed trait is-a BiologicalProcessOrActivity. The replacements are proposed in proposals/metpo_traitmech_v8 and are placeholder ids until METPO mints them.