scholarly journals Out in the midday sun: Repair of UV damage in the Archaea

2004 ◽  
Vol 26 (3) ◽  
pp. 26-29
Author(s):  
Shirley McCready ◽  
Lucio Marcello
Keyword(s):  
Dna Damage ◽  
Uv Irradiation ◽  
Uv Light ◽  
Dna Polymerases ◽  
Life Forms ◽  
Uv Damage ◽  
The Earth ◽  
Lethal Damage ◽  
Living Organisms ◽  
Uv Rays

Living organisms have been exposed to the damaging UV rays in sunlight ever since life began on the Earth, a little over 3.5 billion years ago. Indeed, UV levels on the early Earth's surface were significantly higher than they are now. UV light is absorbed by DNA and causes mutagenic and lethal damage, and today's life forms have evolved a range of strategies for surviving UV irradiation. These include protection from UV (e.g. by pigments, such as melanin, that absorb UV), repair of damaged DNA, and ways of surviving when the damage remains unrepaired (e.g. DNA polymerases that bypass DNA damage).

scholarly journals Preferential repair of UV damage in highly transcribed DNA diminishes UV-induced intrachromosomal recombination in mammalian cells

1994 ◽  
Vol 14 (1) ◽  
pp. 391-399
Author(s):  
W P Deng ◽  
J A Nickoloff
Keyword(s):  
Dna Damage ◽  
Mammalian Cells ◽  
Uv Light ◽  
Uv Damage ◽  
Dna Damage And Repair ◽  
Intrachromosomal Recombination ◽  
Dna Damaging Agents ◽  
Mouse Mammary Tumor ◽  
Tumor Virus ◽  
Virus Promoter

The relationships among transcription, recombination, DNA damage, and repair in mammalian cells were investigated. We monitored the effects of transcription on UV-induced intrachromosomal recombination between neomycin repeats including a promoterless allele and an inducible heteroallele regulated by the mouse mammary tumor virus promoter. Although transcription and UV light separately stimulated recombination, increasing transcription levels reduced UV-induced recombination. Preferential repair of UV damage in transcribed strands was shown in highly transcribed DNA, suggesting that recombination is stimulated by unrepaired UV damage and that increased DNA repair in highly transcribed alleles removes recombinogenic lesions. This study indicates that the genetic consequences of DNA damage depend on transcriptional states and provides a basis for understanding tissue- and gene-specific responses to DNA-damaging agents.

scholarly journals Genetic and physical interactions between Polη and Rev1 in response to UV-induced DNA damage in mammalian cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Tonghui Bi ◽  
Xiaohong Niu ◽  
Chunping Qin ◽  
Wei Xiao
Keyword(s):  
Dna Damage ◽  
Dna Synthesis ◽  
Mammalian Cells ◽  
Damage Tolerance ◽  
Dna Polymerases ◽  
Variant Form ◽  
Physical Interaction ◽  
Uv Damage ◽  
Translesion Dna Synthesis ◽  
Physical Interactions

AbstractIn response to UV irradiation, translesion DNA synthesis (TLS) utilizes specialized DNA polymerases to bypass replication-blocking lesions. In a well-established polymerase switch model, Polη is thought to be a preferred TLS polymerase to insert correct nucleotides across from the thymine dimer, and Rev1 plays a scaffold role through physical interaction with Polη and the Rev7 subunit of Polζ for continual DNA synthesis. Defective Polη causes a variant form of xeroderma pigmentosum (XPV), a disease with predisposition to sunlight-induced skin cancer. Previous studies revealed that expression of Rev1 alone is sufficient to confer enhanced UV damage tolerance in mammalian cells, which depends on its physical interaction with Polζ but is independent of Polη, a conclusion that appears to contradict current literature on the critical roles of Polη in TLS. To test a hypothesis that the Rev1 catalytic activity is required to backup Polη in TLS, we found that the Rev1 polymerase-dead mutation is synergistic with either Polη mutation or the Polη-interaction mutation in response to UV-induced DNA damage. On the other hand, functional complementation of polH cells by Polη relies on its physical interaction with Rev1. Hence, our studies reveal critical interactions between Rev1 and Polη in response to UV damage.

scholarly journals Preferential repair of UV damage in highly transcribed DNA diminishes UV-induced intrachromosomal recombination in mammalian cells.

1994 ◽  
Vol 14 (1) ◽  
pp. 391-399 ◽  
Author(s):  
W P Deng ◽  
J A Nickoloff
Keyword(s):  
Dna Damage ◽  
Mammalian Cells ◽  
Uv Light ◽  
Uv Damage ◽  
Dna Damage And Repair ◽  
Intrachromosomal Recombination ◽  
Dna Damaging Agents ◽  
Mouse Mammary Tumor ◽  
Tumor Virus ◽  
Virus Promoter

The relationships among transcription, recombination, DNA damage, and repair in mammalian cells were investigated. We monitored the effects of transcription on UV-induced intrachromosomal recombination between neomycin repeats including a promoterless allele and an inducible heteroallele regulated by the mouse mammary tumor virus promoter. Although transcription and UV light separately stimulated recombination, increasing transcription levels reduced UV-induced recombination. Preferential repair of UV damage in transcribed strands was shown in highly transcribed DNA, suggesting that recombination is stimulated by unrepaired UV damage and that increased DNA repair in highly transcribed alleles removes recombinogenic lesions. This study indicates that the genetic consequences of DNA damage depend on transcriptional states and provides a basis for understanding tissue- and gene-specific responses to DNA-damaging agents.

A selective, inexpensive probe for UV-induced damage in nucleic acids

2013 ◽  
Vol 91 (5) ◽  
pp. 320-325 ◽  
Author(s):  
Amira F. El-Yazbi ◽  
Glen R. Loppnow
Keyword(s):  
Dna Damage ◽  
Nucleic Acids ◽  
Molecular Beacon ◽  
Uv Light ◽  
Lower Sensitivity ◽  
Uv Damage ◽  
Dna Oligonucleotides ◽  
Dna And Rna ◽  
Hairpin Oligonucleotide ◽  
Hypochromic Effect

Absorption of UV light by nucleic acids can result in the formation of molecular lesions in DNA and RNA, leading to mutagenesis, carcinogenesis, and cell death. In this work, hairpin oligonucleotide probes, which have previously been shown to be selective for DNA damage, are used. The hypochromic effect, which arises from the formation of the target–hairpin hybrid when there is no damage, is used to measure the amount of UV damage by measuring the amount of single-stranded DNA oligonucleotides. With accumulated UV exposure, the target–hairpin hybrid concentration decreases and the absorbance increases, enabling detection of UV-induced DNA damage. Our results show that the selectivity for DNA damage of the hypochromism probe is comparable with the molecular beacon probes, detecting between one and three lesions in an oligonucleotide. In addition, this probe is more than 10 times cheaper than molecular beacon probes. However, it shows lower sensitivity to DNA damage. This makes its use recommended for high-throughput, qualitative analysis of DNA damage. This introduces a simple, fast, mix-and-read assay for the detection of DNA damage.

scholarly journals Formation and Recognition of UV-Induced DNA Damage within Genome Complexity

2020 ◽  
Vol 21 (18) ◽  
pp. 6689
Author(s):  
Philippe Johann to Berens ◽  
Jean Molinier
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Uv Light ◽  
Dna Repair Mechanisms ◽  
Genome Complexity ◽  
Repair Mechanisms ◽  
Living Organisms ◽  
Genomic Regions ◽  
The Impact

Ultraviolet (UV) light is a natural genotoxic agent leading to the formation of photolesions endangering the genomic integrity and thereby the survival of living organisms. To prevent the mutagenetic effect of UV, several specific DNA repair mechanisms are mobilized to accurately maintain genome integrity at photodamaged sites within the complexity of genome structures. However, a fundamental gap remains to be filled in the identification and characterization of factors at the nexus of UV-induced DNA damage, DNA repair, and epigenetics. This review brings together the impact of the epigenomic context on the susceptibility of genomic regions to form photodamage and focuses on the mechanisms of photolesions recognition through the different DNA repair pathways.

scholarly journals Proapoptotic p53-Interacting Protein 53BP2 Is Induced by UV Irradiation but Suppressed by p53

2000 ◽  
Vol 20 (21) ◽  
pp. 8018-8025 ◽  
Author(s):  
Charles D. Lopez ◽  
Yi Ao ◽  
Larry H. Rohde ◽  
Tomas D. Perez ◽  
Daniel J. O'Connor ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Lines ◽  
Uv Irradiation ◽  
Cellular Response ◽  
Clonogenic Survival ◽  
Uv Damage ◽  
Wild Type ◽  
Interacting Protein ◽  
Conditional Expression

ABSTRACT p53 is an important mediator of the cellular stress response with roles in cell cycle control, DNA repair, and apoptosis. 53BP2, a p53-interacting protein, enhances p53 transactivation, impedes cell cycle progression, and promotes apoptosis through unknown mechanisms. We now demonstrate that endogenous 53BP2 levels increase following UV irradiation induced DNA damage in a p53-independent manner. In contrast, we found that the presence of a wild-type (but not mutant) p53 gene suppressed 53BP2 steady-state levels in cell lines with defined p53 genotypes. Likewise, expression of a tetracycline-regulated wild-type p53 cDNA in p53-null fibroblasts caused a reduction in 53BP2 protein levels. However, 53BP2 levels were not reduced if the tetracycline-regulated p53 cDNA was expressed after UV damage in these cells. This suggests that UV damage activates cellular factors that can relieve the p53-mediated suppression of 53BP2 protein. To address the physiologic significance of 53BP2 induction, we utilized stable cell lines with a ponasterone A-regulated 53BP2 cDNA. Conditional expression of 53BP2 cDNA lowered the apoptotic threshold and decreased clonogenic survival following UV irradiation. Conversely, attenuation of endogenous 53BP2 induction with an antisense oligonucleotide resulted in enhanced clonogenic survival following UV irradiation. These results demonstrate that 53BP2 is a DNA damage-inducible protein that promotes DNA damage-induced apoptosis. Furthermore, 53BP2 expression is highly regulated and involves both p53-dependent and p53-independent mechanisms. Our data provide new insight into 53BP2 function and open new avenues for investigation into the cellular response to genotoxic stress.

UV Irradiation Causes the Loss of Viable Mitotic Recombinants in Schizosaccharomyces pombe Cells Lacking the G2/M DNA Damage Checkpoint

Genetics ◽  
2002 ◽  
Vol 160 (3) ◽  
pp. 891-908
Author(s):  
Fekret Osman ◽  
Irina R Tsaneva ◽  
Matthew C Whitby ◽  
Claudette L Doe
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Schizosaccharomyces Pombe ◽  
Uv Irradiation ◽  
Cellular Responses ◽  
Replication Forks ◽  
Uv Damage ◽  
Checkpoint Proteins ◽  
Recombinant Frequency ◽  
Dna Damage Checkpoints

Abstract Elevated mitotic recombination and cell cycle delays are two of the cellular responses to UV-induced DNA damage. Cell cycle delays in response to DNA damage are mediated via checkpoint proteins. Two distinct DNA damage checkpoints have been characterized in Schizosaccharomyces pombe: an intra-S-phase checkpoint slows replication and a G2/M checkpoint stops cells passing from G2 into mitosis. In this study we have sought to determine whether UV damage-induced mitotic intrachromosomal recombination relies on damage-induced cell cycle delays. The spontaneous and UV-induced recombination phenotypes were determined for checkpoint mutants lacking the intra-S and/or the G2/M checkpoint. Spontaneous mitotic recombinants are thought to arise due to endogenous DNA damage and/or intrinsic stalling of replication forks. Cells lacking only the intra-S checkpoint exhibited no UV-induced increase in the frequency of recombinants above spontaneous levels. Mutants lacking the G2/M checkpoint exhibited a novel phenotype; following UV irradiation the recombinant frequency fell below the frequency of spontaneous recombinants. This implies that, as well as UV-induced recombinants, spontaneous recombinants are also lost in G2/M mutants after UV irradiation. Therefore, as well as lack of time for DNA repair, loss of spontaneous and damage-induced recombinants also contributes to cell death in UV-irradiated G2/M checkpoint mutants.

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 Effect of Water Leaching on Photodegraded Scots Pine and Spruce Timbers Monitored by FTIR Spectroscopy

Forests ◽  
2021 ◽  
Vol 12 (7) ◽  
pp. 833
Author(s):  
Edina Preklet ◽  
László Tolvaj ◽  
Eszter Visi-Rajczi ◽  
Tamás Hofmann
Keyword(s):  
Ftir Spectroscopy ◽  
Scots Pine ◽  
Uv Irradiation ◽  
Chemical Elements ◽  
Uv Light ◽  
Carbonyl Groups ◽  
Water Leaching ◽  
Absorption Bands ◽  
Chemical Changes ◽  
Absorption Increase

The goal of this research was the systematic study and comparison of the divided individual effects of UV light irradiation and water leaching during artificial weathering. Spruce (Picea abies Karst.) and Scots pine (Pinus sylvestris L.) samples were irradiated by ultraviolet (UV) light. Another sequence of samples was treated with the combination of UV irradiation and water leaching. The total extent of UV treatment was 20 days for both series of samples. Time relation of UV irradiation and water leaching was 2:1. The chemical changes were observed by FTIR spectroscopy. The difference spectrum was used for determination of the chemical changes. Degradation of lignin was greater for the leached samples than for the pure UV treated samples. Scots pine suffered greater lignin degradation than spruce, and produced higher absorption increase on the absorption region of unconjugated carbonyls. The unconjugated carbonyl groups were the most responsive chemical elements to leaching. Spruce was more susceptible to leaching of unconjugated carbonyl groups than Scots pine. Two absorption bands of unconjugated carbonyl groups at 1706 and 1764 cm−1 wavenumbers were produced by photodegradation. The absorption band at 1764 cm−1 was more sensitive to water leaching than the band at 1706 cm−1.

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