scholarly journals All You Need Is Light. Photorepair of UV-Induced Pyrimidine Dimers

Genes ◽  
2020 ◽  
Vol 11 (11) ◽  
pp. 1304
Author(s):  
Agnieszka Katarzyna Banaś ◽  
Piotr Zgłobicki ◽  
Ewa Kowalska ◽  
Aneta Bażant ◽  
Dariusz Dziga ◽  
...  
Keyword(s):  
Dna Damage ◽  
Uv Light ◽  
High Energy ◽  
Solar Irradiation ◽  
Visible Range ◽  
Special Focus ◽  
Special Importance ◽  
Pyrimidine Dimers ◽  
Uva Light ◽  
Dna Strand

Although solar light is indispensable for the functioning of plants, this environmental factor may also cause damage to living cells. Apart from the visible range, including wavelengths used in photosynthesis, the ultraviolet (UV) light present in solar irradiation reaches the Earth’s surface. The high energy of UV causes damage to many cellular components, with DNA as one of the targets. Putting together the puzzle-like elements responsible for the repair of UV-induced DNA damage is of special importance in understanding how plants ensure the stability of their genomes between generations. In this review, we have presented the information on DNA damage produced under UV with a special focus on the pyrimidine dimers formed between the neighboring pyrimidines in a DNA strand. These dimers are highly mutagenic and cytotoxic, thus their repair is essential for the maintenance of suitable genetic information. In prokaryotic and eukaryotic cells, with the exception of placental mammals, this is achieved by means of highly efficient photorepair, dependent on blue/UVA light, which is performed by specialized enzymes known as photolyases. Photolyase properties, as well as their structure, specificity and action mechanism, have been briefly discussed in this paper. Additionally, the main gaps in our knowledge on the functioning of light repair in plant organelles, its regulation and its interaction between different DNA repair systems in plants have been highlighted.

scholarly journals The Dark Side of UV-Induced DNA Lesion Repair

Genes ◽  
2020 ◽  
Vol 11 (12) ◽  
pp. 1450
Author(s):  
Wojciech Strzałka ◽  
Piotr Zgłobicki ◽  
Ewa Kowalska ◽  
Aneta Bażant ◽  
Dariusz Dziga ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Uv Light ◽  
Genetic Material ◽  
Dna Lesions ◽  
Dark Side ◽  
Repair System ◽  
Strand Breaks ◽  
Dna Lesion ◽  
Pyrimidine Dimers

In their life cycle, plants are exposed to various unfavorable environmental factors including ultraviolet (UV) radiation emitted by the Sun. UV-A and UV-B, which are partially absorbed by the ozone layer, reach the surface of the Earth causing harmful effects among the others on plant genetic material. The energy of UV light is sufficient to induce mutations in DNA. Some examples of DNA damage induced by UV are pyrimidine dimers, oxidized nucleotides as well as single and double-strand breaks. When exposed to light, plants can repair major UV-induced DNA lesions, i.e., pyrimidine dimers using photoreactivation. However, this highly efficient light-dependent DNA repair system is ineffective in dim light or at night. Moreover, it is helpless when it comes to the repair of DNA lesions other than pyrimidine dimers. In this review, we have focused on how plants cope with deleterious DNA damage that cannot be repaired by photoreactivation. The current understanding of light-independent mechanisms, classified as dark DNA repair, indispensable for the maintenance of plant genetic material integrity has been presented.

Experimental Characterization and Modeling of Photon Upconversion in Azobenzene Photomechanical Polymers

2015 ◽  
Author(s):  
Sadiyah Sabah Chowdhury ◽  
Catherine Kent ◽  
Sean P. Hill ◽  
Enric Baduell ◽  
Kenneth Hanson ◽  
...  
Keyword(s):  
Visible Light ◽  
Energy Conversion ◽  
Uv Light ◽  
Green Light ◽  
High Energy ◽  
Photochemical Reactions ◽  
Low Energy ◽  
Mechanical Work ◽  
Solar Irradiation ◽  
Azobenzene Polymer

Azobenzene polymers show promising photostrictive behavior for a broad range of applications in flow control, robotics, and energy harvesting applications. The conversion of solar energy directly into mechanical work provides unique capabilities in adaptive structures; however, the energy conversion of visible light into mechanical work presents several material chemistry challenges. Azobenzene strongly absorbs ultraviolet (UV) light and blue/green light which limits the efficiency of the photomechanical response under solar irradiation. Photon upconversion — combining two or more low energy photons (longer wavelength) to generate a higher energy excited state (shorter wavelength), provides an intriguing strategy to drive these high energy photochemical reactions with low energy light. We present an experimental study showing the feasibility to drive azobenzene photoisomerization using visible light via select up-conversion molecules in the fluidic state. Multi-physics modeling is then used to predict advances in photomechanical energy conversion when up-conversion molecules are introduced within an azobenzene polymer.

scholarly journals Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies

2020 ◽  
Vol 21 (19) ◽  
pp. 7264
Author(s):  
Mateusz Kciuk ◽  
Beata Marciniak ◽  
Mariusz Mojzych ◽  
Renata Kontek
Keyword(s):  
Dna Damage ◽  
Uv Radiation ◽  
Cellular Response ◽  
Current Knowledge ◽  
Uv Light ◽  
Environmental Pollutants ◽  
Ozone Layer ◽  
Special Focus ◽  
Dna Damage And Repair ◽  
Protective Strategies

The protective ozone layer is continually depleting due to the release of deteriorating environmental pollutants. The diminished ozone layer contributes to excessive exposure of cells to ultraviolet (UV) radiation. This leads to various cellular responses utilized to restore the homeostasis of exposed cells. DNA is the primary chromophore of the cells that absorbs sunlight energy. Exposure of genomic DNA to UV light leads to the formation of multitude of types of damage (depending on wavelength and exposure time) that are removed by effectively working repair pathways. The aim of this review is to summarize current knowledge considering cellular response to UV radiation with special focus on DNA damage and repair and to give a comprehensive insight for new researchers in this field. We also highlight most important future prospects considering application of the progressing knowledge of UV response for the clinical control of diverse pathologies.

Riboflavin and UV-Light Based Pathogen Reduction: Extent and Consequence of DNA Damage at the Molecular Level

2004 ◽  
Vol 80 (1) ◽  
pp. 15 ◽  
Author(s):  
Vijay Kumar ◽  
Owen Lockerbie ◽  
Shawn D. Keil ◽  
Patrick H. Ruane ◽  
Matthew S. Platz ◽  
...  
Keyword(s):  
Dna Damage ◽  
Molecular Level ◽  
Uv Light ◽  
Pathogen Reduction

scholarly journals A Role for Histone H2B During Repair of UV-Induced DNA Damage in Saccharomyces cerevisiae

Genetics ◽  
2002 ◽  
Vol 160 (4) ◽  
pp. 1375-1387
Author(s):  
Emmanuelle M D Martini ◽  
Scott Keeney ◽  
Mary Ann Osley
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Chromatin Structure ◽  
Specific Effect ◽  
Cell Killing ◽  
Cyclobutane Pyrimidine Dimers ◽  
Histone H2b ◽  
Uv Sensitivity ◽  
Pyrimidine Dimers

Abstract To investigate the role of the nucleosome during repair of DNA damage in yeast, we screened for histone H2B mutants that were sensitive to UV irradiation. We have isolated a new mutant, htb1-3, that shows preferential sensitivity to UV-C. There is no detectable difference in bulk chromatin structure or in the number of UV-induced cis-syn cyclobutane pyrimidine dimers (CPD) between HTB1 and htb1-3 strains. These results suggest a specific effect of this histone H2B mutation in UV-induced DNA repair processes rather than a global effect on chromatin structure. We analyzed the UV sensitivity of double mutants that contained the htb1-3 mutation and mutations in genes from each of the three epistasis groups of RAD genes. The htb1-3 mutation enhanced UV-induced cell killing in rad1Δ and rad52Δ mutants but not in rad6Δ or rad18Δ mutants, which are defective in postreplicational DNA repair (PRR). When combined with other mutations that affect PRR, the histone mutation increased the UV sensitivity of strains with defects in either the error-prone (rev1Δ) or error-free (rad30Δ) branches of PRR, but did not enhance the UV sensitivity of a strain with a rad5Δ mutation. When combined with a ubc13Δ mutation, which is also epistatic with rad5Δ, the htb1-3 mutation enhanced UV-induced cell killing. These results suggest that histone H2B acts in a novel RAD5-dependent branch of PRR.

scholarly journals The effect of flanking bases on direct and triplet sensitized cyclobutane pyrimidine dimer formation in DNA depends on the dipyrimidine, wavelength and the photosensitizer

2021 ◽  
Author(s):  
Chen Lu ◽  
Natalia Eugenia Gutierrez-Bayona ◽  
John-Stephen Taylor
Keyword(s):  
Uv Light ◽  
Pyrimidine Dimer ◽  
Flanking Sequence ◽  
Quenching Mechanism ◽  
Cyclobutane Pyrimidine Dimers ◽  
Sequence Dependence ◽  
Pyrimidine Dimers ◽  
Skin Cancers ◽  
A Charge ◽  
C To T Mutations

Abstract Cyclobutane pyrimidine dimers (CPDs) are the major products of DNA produced by direct absorption of UV light, and result in C to T mutations linked to human skin cancers. Most recently a new pathway to CPDs in melanocytes has been discovered that has been proposed to arise from a chemisensitized pathway involving a triplet sensitizer that increases mutagenesis by increasing the percentage of C-containing CPDs. To investigate how triplet sensitization may differ from direct UV irradiation, CPD formation was quantified in a 129-mer DNA designed to contain all 64 possible NYYN sequences. CPD formation with UVB light varied about 2-fold between dipyrimidines and 12-fold with flanking sequence and was most frequent at YYYR and least frequent for GYYN sites in accord with a charge transfer quenching mechanism. In contrast, photosensitized CPD formation greatly favored TT over C-containing sites, more so for norfloxacin (NFX) than acetone, in accord with their differing triplet energies. While the sequence dependence for photosensitized TT CPD formation was similar to UVB light, there were significant differences, especially between NFX and acetone that could be largely explained by the ability of NFX to intercalate into DNA.

scholarly journals Repair of DNA Strand Breaks by the Overlapping Functions of Lesion-Specific and Non-Lesion-Specific DNA 3′ Phosphatases

2001 ◽  
Vol 21 (21) ◽  
pp. 7191-7198 ◽  
Author(s):  
John R. Vance ◽  
Thomas E. Wilson
Keyword(s):  
Dna Damage ◽  
Oxidative Dna Damage ◽  
Synthetic Lethality ◽  
Dna Strand Breaks ◽  
Triple Mutant ◽  
Phosphatase Domain ◽  
Strand Breaks ◽  
Alternative Pathways ◽  
Processing Enzymes ◽  
Dna Strand

ABSTRACT In Saccharomyces cerevisiae, the apurinic/apyrimidinic (AP) endonucleases Apn1 and Apn2 act as alternative pathways for the removal of various 3′-terminal blocking lesions from DNA strand breaks and in the repair of abasic sites, which both result from oxidative DNA damage. Here we demonstrate that Tpp1, a homologue of the 3′ phosphatase domain of polynucleotide kinase, is a third member of this group of redundant 3′ processing enzymes. Unlike Apn1 and Apn2, Tpp1 is specific for the removal of 3′ phosphates at strand breaks and does not possess more general 3′ phosphodiesterase, exonuclease, or AP endonuclease activities. Deletion ofTPP1 in an apn1 apn2 mutant background dramatically increased the sensitivity of the double mutant to DNA damage caused by H2O2 and bleomycin but not to damage caused by methyl methanesulfonate. The triple mutant was also deficient in the repair of 3′ phosphate lesions left by Tdp1-mediated cleavage of camptothecin-stabilized Top1-DNA covalent complexes. Finally, the tpp1 apn1 apn2 triple mutation displayed synthetic lethality in combination with rad52, possibly implicating postreplication repair in the removal of unrepaired 3′-terminal lesions resulting from endogenous damage. Taken together, these results demonstrate a clear role for the lesion-specific enzyme, Tpp1, in the repair of a subset of DNA strand breaks.

Factors which affect DNA strand breakage in human leukocytes exposed to a tumor promoter, phorbol myristate acetate

1982 ◽  
Vol 60 (11) ◽  
pp. 1359-1366 ◽  
Author(s):  
H. C. Birnboim
Keyword(s):  
Hydrogen Peroxide ◽  
Dna Damage ◽  
Phorbol Myristate Acetate ◽  
Respiratory Burst ◽  
Superoxide Anion ◽  
Tumor Promoter ◽  
Myristate Acetate ◽  
Strand Breakage ◽  
Dna Strand ◽  
Dna Strand Breakage

We have recently reported that phorbol myristate acetate (PMA) induces extensive DNA strand break damage in human peripheral blood leukocytes. The mechanism of action involves superoxide anion and hydrogen peroxide which are generated by phagocytes during the "respiratory burst." In this report, we describe the effect of various inhibitors and scavengers on PMA-induced DNA damage. Azide and cyanide greatly increased the level of damage; sulfhydryl compounds (glutathione, cysteine, and cysteamine) and ascorbate markedly decreased the level of damage. Hydroxyl radical scavengers such as dimethyl sulfoxide (DMSO) and glycerol also decreased the level of damage but apparently did so by inhibiting the respiratory burst. Diethyldithiocarbamate (DDC) increased the level of DNA damage at low concentrations (<1 mM), but decreased DNA damage at ≥1 mM. The results are consistent with a mechanism involving superoxide anion and hydrogen peroxide, but the precise reaction (free radical or enzymatic) responsible for DNA strand breakage has not been determined. The PMA-stimulated phagocyte is an interesting model system for looking at "active oxygen" mediated DNA damage and factors which influence it.

scholarly journals Engineered Nanoparticles Induce DNA Damage in Primary Human Skin Cells, Even at Low Doses

Nano LIFE ◽  
2014 ◽  
Vol 04 (01) ◽  
pp. 1440001 ◽  
Author(s):  
Amelia A. Romoser ◽  
Michael F. Criscitiello ◽  
Christie M. Sayes
Keyword(s):  
Dna Damage ◽  
Stress Protein ◽  
Dermal Fibroblasts ◽  
Engineered Nanoparticles ◽  
Ros Generation ◽  
Heme Oxygenase 1 ◽  
Dna Double Strand Breaks ◽  
Biological Reduction ◽  
Strand Breaks ◽  
Dna Strand

It is well documented that various particulate matter — either incidental or engineered — are known to generate reactive oxygen species (ROS) in living cells. In circumstances where these reactive species are generated, antioxidant production is often increased. This balance in the biological reduction/oxidation (a.k.a. redox) state within the cell has not been thoroughly studied in exposures involving engineered nanoparticles. However, nanoparticle exposure has been postulated to induce a DNA damage cascade. In this study, we examined primary human dermal fibroblasts (HDF) exposed to three different, but commonly used engineered nanoparticles (i.e., cerium dioxide ( CeO 2), titanium dioxide ( TiO 2) and zinc oxide ( ZnO )) in an attempt to determine the potential DNA damaging effects through the analysis of ROS generation, relevant protein upregulation response and single and double DNA strand breaks. Cell death was most elevated with exposure to ZnO , followed by TiO 2 and CeO 2. ROS generation was measured at 1 h, 6 h and 24 h after exposure to particles via a cell-based DCFH-DA (2′, 7′-dichlorfluorescein-diacetate) assay and indicated that ZnO generated the most significant amount of ROS. ZnO also caused upregulation of oxidative stress protein, heme oxygenase-1 and phosphorylation of p38; whereas CeO 2 caused upregulation of superoxide dismutase. Results from the comet assay indicated that ZnO triggered significant DNA damage in cells at relatively low dosing concentrations (20 ppm). Immunocytochemistry with ZnO -treated cells revealed notable DNA double strand breaks evidenced by a marked increase in the presence of γ-H2AX foci. This finding was also indicated by western blot, as well as cell cycle arrest by the phosphorylation of cyclin-dependent kinase 1. These data suggest that the three particle-types induce different degrees of DNA damage. And, of the three particle-types tested, exposure to ZnO nanoparticles may cause the most significant DNA damage.

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