Accumulation Of Cyclobutane Pyrimidine Dimers Research Articles

Dynamic accumulation of cyclobutane pyrimidine dimers and its response to changes in DNA conformation.

Photochemical dimerization of adjacent pyrimidines is fundamental to the creation of mutagenic hotspots caused by ultraviolet light. Distribution of the resulting lesions (cyclobutane pyrimidine dimers, CPDs) is already known to be highly variable in cells, and in vitro models have implicated DNA conformation as a major basis for this observation. Past efforts have primarily focused on mechanisms that influence CPD formation and have rarely considered contributions of CPD reversion. However, reversion is competitive under the standard conditions of 254 nm irradiation as illustrated in this report based on the dynamic response of CPDs to changes in DNA conformation. A periodic profile of CPDs was recreated in DNA held in a bent conformation by λ repressor. After linearization of this DNA, the CPD profile relaxed to its characteristic uniform distribution over a similar time of irradiation to that required to generate the initial profile. Similarly, when a T tract was released from a bent conformation, its CPD profile converted under further irradiation to that consistent with a linear T tract. This interconversion of CPDs indicates thatboth its formation and reversion exert control on CPD populations long before photo-steady-state conditions are achieved and suggests that the dominant sites of CPDs will evolve as DNA conformation changes in response to natural cellular processes.

Reduction of DNA damage repair efficiency and accumulation of residual damage following chronic UVB-irradiation of HaCaT cells.

Absorption of ultraviolet radiation (UVR) by DNA leads to the predominant formation of cyclobutane pyrimidine dimers (CPD). Since those CPD are responsible for the driver mutations found in skin cancers, their efficient repair is critical. We previously showed that pre-stimulation of fibroblasts with chronic low doses of UVB (CLUV) increases CPD repair efficiency. Since skin cancers are not arising from dermal fibroblasts, this observation is not directly relevant to cutaneous carcinogenesis. We have now exposed HaCaT keratinocytes to a CLUV irradiation protocol to determine whether this pre-stimulation influences CPD removal rate. Similar to fibroblasts, CLUV treatment leads to the accumulation of residual CPD in keratinocytes, which are not repaired but rather tolerated and diluted through DNA replication. In contrast to fibroblasts, in keratinocytes we find that CLUV pre-treatment reduces CPD removal of newly generated damage without inducing a higher sensitivity to UVR-induced cell death. Using our experimental data, we derived a theoretical model to predict CPD induction, dilution and repair that occur in keratinocytes when chronically UVB-irradiated. Altogether, these results suggest that the accumulation of unrepaired CPD and the reduction in repair efficiency caused by chronic UVB exposure might lead to an increase in skin cancer driver mutations.

UV-B-Induced CPD Photolyase Gene Expression is Regulated by UVR8-Dependent and -Independent Pathways in Arabidopsis.

Plants have evolved various mechanisms that protect against the harmful effects of UV-B radiation (280-315 nm) on growth and development. Cyclobutane pyrimidine dimer (CPD) photolyase, the repair enzyme for UV-B-induced CPDs, is essential for protecting cells from UV-B radiation. Expression of the CPD photolyase gene (PHR) is controlled by light with various wavelengths including UV-B, but the mechanisms of this regulation remain poorly understood. In this study, we investigated the regulation of PHR expression by light with various wavelengths, in particular low-fluence UV-B radiation (280 nm, 0.2 µmol m-2 s -1), in Arabidopsis thaliana seedlings grown under light-dark cycles for 7 d and then adapted to the dark for 3 d. Low-fluence UV-B radiation induced CPDs but not reactive oxygen species. AtPHR expression was effectively induced by UV-B, UV-A (375 nm) and blue light. Expression induced by UV-A and blue light was predominantly regulated by the cryptochrome-dependent pathway, whereas phytochromes A and B played a minor but noticeable role. Expression induced by UV-B was predominantly regulated by the UVR8-dependent pathway. AtPHR expression was also mediated by a UVR8-independent pathway, which is correlated with CPD accumulation induced by UV-B radiation. These results indicate that Arabidopsis has evolved diverse mechanisms to regulate CPD photolyase expression by multiple photoreceptor signaling pathways, including UVR8-dependent and -independent pathways, as protection against harmful effects of UV-B radiation.

AtCAF-1 mutants show different DNA damage responses after ultraviolet-B than those activated by other genotoxic agents in leaves.

Chromatin assembly factor-1 (CAF-1) is a histone H3/H4 chaperone that participates in DNA and chromatin interaction processes. In this manuscript, we show that organs from CAF-1 deficient plants respond differently to ultraviolet-B (UV-B) radiation than to other genotoxic stresses. For example, CAF-1 deficient leaves tolerate better UV-B radiation, showing lower cyclobutane pyrimidine dimer (CPD) accumulation, lower inhibition of cell proliferation, increased cell wall thickness, UV-B absorbing compounds, and ploidy levels, whereas previous data from different groups have shown that CAF-1 mutants show shortening of telomeres, loss of 45S rDNA, and increased homologous recombination, phenotypes associated to DNA breaks. Interestingly, CAF-1 deficient roots show increased inhibition of primary root elongation, with decreased meristem size due to a higher inhibition of cell proliferation after UV-B exposure. The decrease in root meristem size in CAF-1 mutants is a consequence of defects in programmed cell death after UV-B exposure. Together, we provide evidence demonstrating that root and shoot meristematic cells may have distinct protection mechanisms against CPD accumulation by UV-B, which may be linked with different functions of the CAF-1 complex in these different organs.

EFFECTOR OF TRANSCRIPTION factors are novel plant-specific regulators associated with genomic DNA methylation in Arabidopsis.

Summary Plant‐specific EFFECTORS OF TRANSCRIPTION (ET) are characterised by a variable number of highly conserved ET repeats, which are involved in zinc and DNA binding. In addition, ETs share a GIY‐YIG domain, involved in DNA nicking activity. It was hypothesised that ETs might act as epigenetic regulators.Here, methylome, transcriptome and phenotypic analyses were performed to investigate the role of ET factors and their involvement in DNA methylation in Arabidopsis thaliana.Comparative DNA methylation and transcriptome analyses in flowers and seedlings of et mutants revealed ET‐specific differentially expressed genes and mostly independently characteristic, ET‐specific differentially methylated regions. Loss of ET function results in pleiotropic developmental defects.The accumulation of cyclobutane pyrimidine dimers after ultraviolet stress in et mutants suggests an ET function in DNA repair.

Persistence and Tolerance of DNA Damage Induced by Chronic UVB Irradiation of the Human Genome

Exposure to solar UVB radiation leads to the formation of the highly mutagenic cyclobutane pyrimidine dimers (CPDs), the DNA damage responsible for mutations found in skin cancer. The frequency of CPD formation and the repair rate of those lesions are two important parameters to determine the probability of UVR-induced mutations. Previous work has shown that chronic irradiation with sublethal doses of UVB radiation (chronic low-dose UVB radiation) leads to the accumulation of residual CPD that persists over time. We have thus investigated the persistence, localization, and consequences on genome stability of those chronic low-dose UVB radiation-induced residual CPDs. We show that chronic low-dose UVB radiation-induced residual CPDs persist on DNA and are diluted via semiconservative replication. They are overrepresented in the heterochromatin and at the TT dipyrimidine sites, and they catalyze the incidence of sister chromatin exchange. Our results shed some light on the impact of chronic UVB radiation exposure on DNA, with a focus on residual CPDs, their distribution, and consequences.

Insight in DNA Repair of UV-induced Pyrimidine Dimers by Chromatographic Methods.

UV-induced formation of pyrimidine dimers in DNA is a major deleterious event in both eukaryotic and prokaryotic cells. Accumulation of cyclobutane pyrimidine dimers and pyrimidine (6-4) pyrimidone photoproducts can lead to cell death or be at the origin of mutations. In skin, UV induction of DNA damage is a major initiating event in tumorigenesis. To counteract these deleterious effects, all cell types possess DNA repair machinery, such as nucleotide excision repair and, in some cell types, direct reversion. Different analytical approaches were used to assess the efficiency of repair and decipher the enzymatic mechanisms. We presently review the information provided by chromatographic methods, which are complementary to biochemical assays, such as immunological detection and electrophoresis-based techniques. Chromatographic assays are interesting in their ability to provide quantitative data on a wide range of damage and are also valuable tools for the identification of repair intermediates.

Influence of exogenous silicon on UV-B radiation-induced cyclobutane pyrimidine dimmers in soybean leaves and its alleviation mechanism

The DNA is particularly sensitive to UV-B radiation and can readily be damaged by UV-B stress, resulting to the formation of photoproducts like cyclobutane pyrimidine dimers (CPDs). Silicon has multifarious benefits to plants, especially under biotic and abiotic stress. In this study, we used soybean seedlings to determine whether silicon could alleviate damage to DNA caused by UV-B stress. Silicon significantly reduced the accumulation of CPDs, lessening the damage of UV-B stress to the seedlings by the following three mechanisms: (1) increasing the concentration of UV-B absorbing compounds to reduce damage; (2) strengthening the antioxidant capacity of plants represented by higher levels of non-enzymatic antioxidants and (3) increasing the photolyase gene expression, thus accelerating photorepair.

UV-B-Induced CPD Photolyase Gene Expression is Regulated by UVR8-Dependent and -Independent Pathways in Arabidopsis.

Plants have evolved various mechanisms that protect against the harmful effects of UV-B radiation (280-315 nm) on growth and development. Cyclobutane pyrimidine dimer (CPD) photolyase, the repair enzyme for UV-B-induced CPDs, is essential for protecting cells from UV-B radiation. Expression of the CPD photolyase gene (PHR) is controlled by light with various wavelengths including UV-B, but the mechanisms of this regulation remain poorly understood. In this study, we investigated the regulation of PHR expression by light with various wavelengths, in particular low-fluence UV-B radiation (280 nm, 0.2 µmol m(-2) s(-1)), in Arabidopsis thaliana seedlings grown under light-dark cycles for 7 d and then adapted to the dark for 3 d. Low-fluence UV-B radiation induced CPDs but not reactive oxygen species. AtPHR expression was effectively induced by UV-B, UV-A (375 nm) and blue light. Expression induced by UV-A and blue light was predominantly regulated by the cryptochrome-dependent pathway, whereas phytochromes A and B played a minor but noticeable role. Expression induced by UV-B was predominantly regulated by the UVR8-dependent pathway. AtPHR expression was also mediated by a UVR8-independent pathway, which is correlated with CPD accumulation induced by UV-B radiation. These results indicate that Arabidopsis has evolved diverse mechanisms to regulate CPD photolyase expression by multiple photoreceptor signaling pathways, including UVR8-dependent and -independent pathways, as protection against harmful effects of UV-B radiation.

A functional single‐nucleotide polymorphism in the ERCC 1 gene alters the efficacy of narrowband ultraviolet B therapy in patients with active vitiligo in a Chinese population

T lymphocytes have been shown to cause the destruction of melanocytes in vitiligo pathogenesis. Narrowband ultraviolet B (NB-UVB), as an effective therapeutic strategy in vitiligo, can lead to the formation of DNA photoproducts such as cyclobutane pyrimidine dimers (CPDs) in perilesional lymphocytes and thus induce skin immunosuppression. The repair of DNA photoproducts is performed mainly through the nucleotide excision repair (NER) pathway. We hypothesized that single-nucleotide polymorphisms (SNPs) in NER genes might influence the repair capacity of CPDs and thus contribute to variations in phototherapy efficiency. To detect genetic polymorphisms in NER genes and their relationship with the efficacy of NB-UVB therapy in patients with active vitiligo. We investigated the association of NER SNPs (XPA A23G, XPC Ci11A, XPC C2919A and ERCC1 C118T) with phototherapy efficacy in 86 patients with vitiligo who received NB-UVB treatment. Furthermore, we examined the impact of ERCC1 C118T on the apoptosis of T lymphocytes and CPD accumulation after NB-UVB irradiation. We found that patients with vitiligo with the ERCC1 codon 118 CC genotype showed better efficacy after NB-UVB irradiation than those with the ERCC1 118 TT and CT genotypes, whereas no such association was documented among the genotypes of XPA A23G, XPC Ci11A or XPC C2919A. Additionally, the apoptosis rates and CPD levels of lymphocytes after NB-UVB irradiation in patients with the ERCC1 118 CC genotype were significantly higher than those in patients with the ERCC1 118 TT and CT genotypes. The ERCC1 118 CC genotype confers better efficacy of NB-UVB therapy in patients with active vitiligo.

Diurnal variation in bacterioplankton composition and DNA damage in the microbial community from an Andean oligotrophic lake

Laguna Azul is an oligotrophic lake situated at 4,560m above sea level and subject to a high level of solar radiation. Bacterioplankton community composition (BCC) was analysed by denaturing gradient gel electrophoresis and the impact of solar ultraviolet radiation was assessed by measuring cyclobutane pyrimidine dimers (CPD). Furthermore, pure cultures of Acinetobacter johnsonii A2 and Rhodococcus sp. A5 were exposed simulta-neously and CPD accumulation was studied. Gel analyses generated a total of 7 sequences belonging to Alpha-proteobacteria (1 band), Beta-proteobacteria (1 band), Bacteroidetes (2 bands), Actinobacteria (1 band), and Firmicutes (1 band). DGGE profiles showed minimal changes in BCC and no CPD was detected even though a high level of damage was found in biodosimeters. A. johnsonii A2 showed low level of DNA damage while Rhodococcus sp. A5 exhibited high resistance since no CPD were detected under natural UV-B exposure, suggesting that the bacterial community is well adapted to this highly solar irradiated environment.

Elevated CO2 alleviates high PAR and UV stress in the unicellular chlorophyte Dunaliella tertiolecta.

The effects of increased CO2 and irradiance on the physiological performance of the chlorophyte Dunaliella tertiolecta were studied at different PAR and UVR (UVA + UVB) irradiances, simulating the solar radiation at different depths, at present (390 ppmv, LC) and predicted CO2 levels for the year 2100 (1000 ppmv, HC). Elevated CO2 resulted in higher optimum and effective quantum yields (F(v)/F(m) and ϕPSII, respectively), electron transport rates (ETR) and specific growth rates (μ). Cell stress was alleviated in HC with respect to LC as evidenced by a decrease in reactive oxygen species (ROS) accumulation. DNA damage showed a 42-fold increase in cyclobutane-pyrimidine dimer (CPD) formation under the highest irradiance (1100 μmol quanta m(-2) s(-1)) in LC with respect to the lowest irradiance (200 μmol quanta m(-2) s(-1)). Photolyase (CII-PCD-PL) gene expression was upregulated under HC resulting in a drastic decrease in CPD accumulation to only 25% with respect to LC. Proliferating cell nuclear antigen (PCNA) accumulation was always higher in HC and the accumulation pattern indicated its involvement in repair or growth depending on the irradiance dose. The repressor of silencing (ROS1) was only marginally involved in the response, suggesting that photoreactivation was the most relevant mechanism to overcome UVR damage. Our results demonstrate that future scenarios of global change result in alleviation of irradiance stress by CO2-induced photoprotection in D. tertiolecta.

UVB-induced DNA and photosystem II damage in two intertidal green macroalgae: Distinct survival strategies in UV-screening and non-screening Chlorophyta

Ultraviolet-B-induced (UVB, 280–315nm) accumulation of cyclobutane pyrimidine dimers (CPDs) and deactivation of photosystem II (PS II) was quantified in two intertidal green macroalgae, Ulva clathrata and Rhizoclonium riparium. The species were chosen due to their shared habitats but contrasting UVB screening potentials. In the non-screening U. clathrata CPDs accumulated and PS II activity declined as a linear function of applied UVB irradiance. In R. riparium UVB-induced damage was significantly lower than in U. clathrata, demonstrating an efficient UVB protection of DNA and PS II by screening. Based on the UVB irradiance reaching the chloroplasts, both species showed an identical intrinsic sensitivity of PS II towards UVB, but DNA lesions accumulated slower in U. clathrata. While repair of CPDs was similar in both species, U. clathrata was capable of restoring its PS II function decidedly faster than R. riparium. In R. riparium efficient screening may represent an adaptation to its high light habitat, whereas in U. clathrata high repair rates of PS II appear to be important to survive natural UVB exposure. The role of shading of the nucleus by the large chloroplasts in U. clathrata is discussed.

Participation of chromatin-remodeling proteins in the repair of ultraviolet-B-damaged DNA.

The genome of plants is organized into chromatin, affecting the rates of transcription, DNA recombination, and repair. In this work, we have investigated the consequences of reduced expression of some chromatin-remodeling factors and histone acetylation in maize (Zea mays) and Arabidopsis (Arabidopsis thaliana) in their participation in DNA repair after ultraviolet (UV)-B irradiation. Plants deficient in NFC102/NFC4 or SDG102/SDG26 showed more damaged DNA than wild-type plants; however, the Arabidopsis chc1 mutant showed similar accumulation of cyclobutane pyrimidine dimers as wild-type plants, in contrast to the increased DNA damage measured in the maize chc101 RNA interference line. In Arabidopsis, plants deficient in chromatin remodeling are also affected in the accumulation of pigments by UV-B. Plants treated with an inhibitor of histone acetyltransferases, curcumin, previous to the UV-B treatment show deficiencies in DNA repair; in addition, the chromatin remodeling-deficient plants have altered levels of acetylated histones after the UV-B treatment, demonstrating that histone acetylation is important during DNA repair in these two plant species. Arabidopsis mutants ham1 and ham2 also showed increased DNA damage after UV-B, suggesting that the role of these proteins in DNA damage repair has been conserved through evolution. However, cyclobutane pyrimidine dimer accumulation was higher in ham1 than in ham2; suggesting that HAM1 has a major role in DNA repair after UV-B. In summary, in this work, we have demonstrated that chromatin remodeling, and histone acetylation in particular, is important during DNA repair by UV-B, demonstrating that both genetic and epigenetic effects control DNA repair in plants.

UVB Photoprotective Role of Mycosporines in Yeast: Photostability and Antioxidant Activity of Mycosporine-Glutaminol-Glucoside

Several yeast species are able to synthesize and accumulate UV-radiation-absorbing mycosporine metabolites that are of unclear physiological function. In this work we analyzed the relationship between mycosporine-glutaminol glucoside (MGG) production, cell survival after UVB irradiation, and formation of cyclobutane pyrimidine dimers (CPDs). We also assessed the photostability and singlet oxygen quenching activity of MGG. A set of nine isolates of the basidiomycetous yeast Cryptococcus steppossus cultured in both dark and light conditions was used for the studies. Survival of the UVB-irradiated isolates and MGG concentration had a linear relationship when the concentration was over 2.5 mg g(-1). CPD accumulation and MGG accumulation were inversely related. MGG in aqueous solution was photostable with a photodecomposition quantum yield of 1.16 × 10(-5). MGG quenching of singlet oxygen was also observed, and the rate constant for the process in D(2)O was 5.9 × 10(7) M(-1) s(-1). Our results support the idea that MGG plays an important role as a UVB photoprotective metabolite in yeasts by protecting against direct damage on DNA and probably against indirect damage by singlet oxygen quenching.

Assessment of UV-B damage in cyanophage PP

AME Aquatic Microbial Ecology Contact the journal Facebook Twitter RSS Mailing List Subscribe to our mailing list via Mailchimp HomeLatest VolumeAbout the JournalEditorsSpecials AME 58:323-328 (2010) - DOI: https://doi.org/10.3354/ame01386 Assessment of UV-B damage in cyanophage PP Ming-Jun Liao1,2,3, Kai Cheng2, Jiao-Yan Yang2, Yi-Jun Zhao2,*, Zheng-Li Shi1,** 1State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, PR China 2Hubei Key Laboratory of Urban Water Environmental Ecology, Central China Normal University, Wuhan 430079, PR China 3Graduate School of Chinese Academy of Sciences, Beijing 100039, PR China Corresponding authors. Email: *zhaoyj@mail.ccnu.edu.cn; **zlshi@wh.iov.cn ABSTRACT: Cyanophage PP is a short-tailed, icosahedral-shaped, double-stranded DNA virus and can be frequently detected with high abundance and activity in many eutrophic lakes in China. Solar radiation is one of the main factors affecting cyanophage infectivity. In this study, cyanophage PP was treated with different intensities of UV-B radiation, and the accumulation of cyclobutane pyrimidine dimers (CPDs), viral particle destruction and viral attachment ability were analyzed. The viral infectivity decay rate under white and red light was also studied using plaque-forming assays. The results indicate that (1) the level of CPDs induced by UV-B was significantly correlated with radiation intensity, while exposure dose had little effect on the DNA damage level, (2) the level of CPDs was significantly correlated with both the decay rate and the repair rate in cyanophage PP, and (3) UV-B could result in the destruction of viral particles and the decrease in viral attachment. This work suggests that the secondary and tertiary structure of the DNA may influence the formation of CPDs, and that capsid damage caused by UV-B radiation may play an important role in viral decay and survival. KEY WORDS: Cyanophage PP · UV-B · Cyclobutane pyrimidine dimers · CPDs · Capsid damage Full text in pdf format PreviousCite this article as: Liao MJ, Cheng K, Yang JY, Zhao YJ, Shi ZL (2010) Assessment of UV-B damage in cyanophage PP. Aquat Microb Ecol 58:323-328. https://doi.org/10.3354/ame01386 Export citation RSS - Facebook - Tweet - linkedIn Cited by Published in AME Vol. 58, No. 3. Online publication date: February 11, 2010 Print ISSN: 0948-3055; Online ISSN: 1616-1564 Copyright © 2010 Inter-Research.

Impact of solar radiation on bacterioplankton in Laguna Vilama, a hypersaline Andean lake (4650 m)

Laguna Vilama is a hypersaline Lake located at 4660 m altitude in the northwest of Argentina high up in the Andean Puna. The impact of ultraviolet (UV) radiation on bacterioplankton was studied by collecting samples at different times of the day. Molecular analysis (DGGE) showed that the bacterioplankton community is characterized by Gamma‐proteobacteria (Halomonas sp., Marinobacter sp.), Alpha‐proteobacteria (Roseobacter sp.), HGC (Agrococcus jenensis and an uncultured bacterium), and CFB (uncultured Bacteroidetes). During the day, minor modifications in bacterial diversity such as intensification of Bacteroidetes' signal and an emergence of Gamma‐proteobacteria (Marinobacter flavimaris) were observed after solar exposure. DNA damage, measured as an accumulation of Cyclobutane Pyrimidine Dimers (CPDs), in bacterioplankton and naked DNA increased from 100 CPDs MB−1 at 1200 local time (LT) to 300 CPDs MB−1 at 1600 LT, and from 80 CPDs MB−1 at 1200 LT to 640 CPDs MB−1 at 1600 LT, respectively. In addition, pure cultures of Pseudomonas sp. V1 and Brachybacterium sp. V5, two bacteria previously isolated from this environment, were exposed simultaneously with the community, and viability of both strains diminished after solar exposure. No CPD accumulation was observed in either of the exposed cultures, but an increase in mutagenesis was detected in V5. Of both strains only Brachybacterium sp. V5 showed CPD accumulation in naked DNA. These results suggest that the bacterioplankton community is well adapted to this highly solar irradiated environment showing little accumulation of CPDs and few changes in the community composition. They also demonstrate that these microorganisms contain efficient mechanisms against UV damage.

Accumulation of DNA damage in Antarctic mosses: correlations with ultraviolet‐B radiation, temperature and turf water content vary among species

AbstractThe susceptibility of three East Antarctic moss species to UV‐B radiation was examined by measuring accumulation of cyclobutane pyrimidine dimers under natural sunlight during the austral summer season of 2002/03. The 2002/03 season was characterized by unusually low springtime ozone depletion and as such our results likely underestimate the DNA damage possible in a more typical UV‐B radiation season. Despite this all three species accumulated significant DNA photoproducts. We also found a positive association between photoproduct accumulation and incident UV‐B radiation in the two cosmopolitan species, Bryum pseudotriquetrum and Ceratodon purpureus, with more DNA damage in samples collected early in the season compared with later in the summer. For B. pseudotriquetrum, negative associations were also observed between photoproduct accumulation and both turf water content and the 10‐day mean air temperature. Photoproduct accumulation in the endemic species Schistidium antarctici was similarly high across the season and no significant association with environmental variables was found. Our results are consistent with the two cosmopolitan species having somewhat higher UV‐B‐screening capabilities and possibly more efficient mechanisms for repairing DNA damage than the endemic S. antarctici.

Desiccation protects two Antarctic mosses from ultraviolet-B induced DNA damage.

Antarctic mosses live in a frozen desert, and are characterised by the ability to survive desiccation. They can tolerate multiple desiccation-rehydration events over the summer growing season. As a result of recent ozone depletion, such mosses may also be exposed to ultraviolet-B radiation while desiccated. The ultraviolet-B susceptibility of Antarctic moss species was examined in a laboratory experiment that tested whether desiccated or hydrated mosses accumulated more DNA damage under enhanced ultraviolet-B radiation. Accumulation of cyclobutane pyrimidine dimers and pyrimidine (6-4) pyrimidone dimers was measured in moss samples collected from the field and then exposed to ultraviolet-B radiation in either a desiccated or hydrated state. Two cosmopolitan species, Ceratodon purpureus (Hedw.) Brid. and Bryum pseudotriquetrum (Hedw.) Gaertn., B.Mey. & Scherb, were protected from DNA damage when desiccated, with accumulation of cyclobutane pyrimidine dimers reduced by at least 60% relative to hydrated moss. The endemic Schistidium antarctici (Cardot) L.I. Savicz & Smirnova accumulated more DNA damage than the other species and desiccation was not protective in this species. The cosmopolitan species remarkable ability to tolerate high ultraviolet-B exposure, especially in the desiccated state, suggests they may be better able to tolerate continued elevated ultraviolet-B radiation than the endemic species.

UVR-induced photosynthetic inhibition dominates over DNA damage in marine dinoflagellates exposed to fluctuating solar radiation regimes

The combined effect of solar radiation (UV-B (280-315 nm), UV-A (315-400 nm) and PAR (400-700 nm)) and vertical mixing (i.e., fluctuating radiation regimes) on the marine dinoflagellates Gymnodinium chlorophorum, Heterocapsa triquetra and Prorocentrum micans was investigated during the austral spring in Patagonia, Argentina. Photosynthesis, measured as radiocarbon incorporation, and accumulation of DNA damage, as cyclobutane pyrimidine dimers (CPDs), were investigated under simulated mixed and non-mixed water column conditions using 3 h incubations centered at local noon. Static samples had significant UVR-induced photoinhibition that was higher in H. triquetra as compared to the other two species. Increasing mixing speed significantly increased UVR-induced inhibition of carbon fixation in G. chlorophorum and H. triquetra. No significant UVR effect was observed in P. micans under any of the mixing regimes. Most of the loss in carbon fixation in G. chlorophorum was due to UV-B while in H. triquetra it was due to UV-A. Part of these responses may be associated to the presence of UV-absorbing compounds which were abundant in P. micans, and low in H. triquetra and in G. chlorophorum. However, other variables such as cell size and active repair might have also influenced our results. We did not detect CPD accumulation in any of the species, probably because of the low solar angle that resulted in very low levels of DNA effective UV-B dose. Our results indicate that exposure to solar UVR in the Patagonia area during spring time (even during ozone depletion events) has a clear impact on photosynthesis and much less or negligible on DNA in the three studied species.