scholarly journals Exciton Absorption and Luminescence in i-Motif DNA

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Zakhar V. Reveguk ◽  
Evgeny V. Khoroshilov ◽  
Andrey. V. Sharkov ◽  
Vladimir A. Pomogaev ◽  
Andrey A. Buglak ◽  
...  
Keyword(s):  
Excited State ◽  
Energy Transition ◽  
Dna Lesions ◽  
Time Range ◽  
Cyclobutane Pyrimidine Dimers ◽  
Excited State Dynamics ◽  
Experimental Absorption Spectrum ◽  
Pyrimidine Dimers ◽  
Electronic Transition Energies ◽  
Experimental Absorption

Abstract We have studied the excited-state dynamics for the i-motif form of cytosine chains (dC)10, using the ultrafast fluorescence up-conversion technique. We have also calculated vertical electronic transition energies and determined the nature of the corresponding excited states in a model tetramer i-motif structure. Quantum chemical calculations of the excitation spectrum of a tetramer i-motif structure predict a significant (0.3 eV) red shift of the lowest-energy transition in the i-motif form relative to its absorption maximum, which agrees with the experimental absorption spectrum. The lowest excitonic state in i-(dC)10 is responsible for a 2 ps red-shifted emission at 370 nm observed in the decay-associated spectra obtained on the femtosecond time-scale. This delocalized (excitonic) excited state is likely a precursor to a long-lived excimer state observed in previous studies. Another fast 310 fs component at 330 nm is assigned to a monomer-like locally excited state. Both emissive states form within less than the available time resolution of the instrument (100 fs). This work contributes to the understanding of excited-state dynamics of DNA within the first few picoseconds, which is the most interesting time range with respect to unraveling the photodamage mechanism, including the formation of the most dangerous DNA lesions such as cyclobutane pyrimidine dimers.

scholarly journals Cyclobutane pyrimidine dimers are predominant DNA lesions in whole human skin exposed to UVA radiation

2006 ◽  
Vol 103 (37) ◽  
pp. 13765-13770 ◽  
Author(s):  
S. Mouret ◽  
C. Baudouin ◽  
M. Charveron ◽  
A. Favier ◽  
J. Cadet ◽  
...  
Keyword(s):  
Human Skin ◽  
Dna Lesions ◽  
Cyclobutane Pyrimidine Dimers ◽  
Pyrimidine Dimers ◽  
Uva Radiation

scholarly journals Two Photolyases Repair Distinct DNA Lesions and Reactivate UVB-Inactivated Conidia of an Insect Mycopathogen under Visible Light

2018 ◽  
Vol 85 (4) ◽  
Author(s):  
Ding-Yi Wang ◽  
Bo Fu ◽  
Sen-Miao Tong ◽  
Sheng-Hua Ying ◽  
Ming-Guang Feng
Keyword(s):  
Visible Light ◽  
Beauveria Bassiana ◽  
Type Strain ◽  
Wild Type Strain ◽  
Dna Lesions ◽  
Wild Type ◽  
Cyclobutane Pyrimidine Dimers ◽  
Content Type ◽  
Uvb Irradiation ◽  
Pyrimidine Dimers

ABSTRACT Fungal conidia serve as active ingredients of fungal insecticides but are sensitive to solar UV irradiation, which impairs double-stranded DNA (dsDNA) by inducing the production of cytotoxic cyclobutane pyrimidine dimers (CPDs) and (6-4)-pyrimidine-pyrimidine photoproducts (6-4PPs). This study aims to elucidate how CPD photolyase (Phr1) and 6-4PP photolyase (Phr2) repair DNA damage and photoreactivate UVB-inactivated cells in Beauveria bassiana, a main source of fungal insecticides. Both Phr1 and Phr2 are proven to exclusively localize in the fungal nuclei. Despite little influence on growth, conidiation, and virulence, singular deletions of phr1 and phr2 resulted in respective reductions of 38% and 19% in conidial tolerance to UVB irradiation, a sunlight component most harmful to formulated conidia. CPDs and 6-4PPs accumulated significantly more in the cells of Δphr1 and Δphr2 mutants than in those of a wild-type strain under lethal UVB irradiation and were largely or completely repaired by Phr1 in the Δphr2 mutant and Phr2 in the Δphr1 mutant after optimal 5-h exposure to visible light. Consequently, UVB-inactivated conidia of the Δphr1 and Δphr2 mutants were much less efficiently photoreactivated than were the wild-type counterparts. In contrast, overexpression of either phr1 or phr2 in the wild-type strain resulted in marked increases in both conidial UVB resistance and photoreactivation efficiency. These findings indicate essential roles of Phr1 and Phr2 in photoprotection of B. bassiana from UVB damage and unveil exploitable values of both photolyase genes for improved UVB resistance and application strategy of fungal insecticides. IMPORTANCE Protecting fungal cells from damage from solar UVB irradiation is critical for development and application of fungal insecticides but is mechanistically not understood in Beauveria bassiana, a classic insect pathogen. We unveil that two intranuclear photolyases, Phr1 and Phr2, play essential roles in repairing UVB-induced dsDNA lesions through respective decomposition of cytotoxic cyclobutane pyrimidine dimers and (6-4)-pyrimidine-pyrimidine photoproducts, hence reactivating UVB-inactivated cells effectively under visible light. Our findings shed light on the high potential of both photolyase genes for use in improving UVB resistance and application strategy of fungal insecticides.

scholarly journals An alternative eukaryotic DNA excision repair pathway.

1995 ◽  
Vol 15 (8) ◽  
pp. 4572-4577 ◽  
Author(s):  
G A Freyer ◽  
S Davey ◽  
J V Ferrer ◽  
A M Martin ◽  
D Beach ◽  
...  
Keyword(s):  
Dna Repair ◽  
Excision Repair ◽  
Uv Light ◽  
Repair Process ◽  
Dna Lesions ◽  
Repair Pathway ◽  
Cyclobutane Pyrimidine Dimers ◽  
Dna Excision Repair ◽  
Pyrimidine Dimers

DNA lesions induced by UV light, cyclobutane pyrimidine dimers, and (6-4)pyrimidine pyrimidones are known to be repaired by the process of nucleotide excision repair (NER). However, in the fission yeast Schizosaccharomyces pombe, studies have demonstrated that at least two mechanisms for excising UV photo-products exist; NER and a second, previously unidentified process. Recently we reported that S. pombe contains a DNA endonuclease, SPDE, which recognizes and cleaves at a position immediately adjacent to cyclobutane pyrimidine dimers and (6-4)pyrimidine pyrimidones. Here we report that the UV-sensitive S. pombe rad12-502 mutant lacks SPDE activity. In addition, extracts prepared from the rad12-502 mutant are deficient in DNA excision repair, as demonstrated in an in vitro excision repair assay. DNA repair activity was restored to wild-type levels in extracts prepared from rad12-502 cells by the addition of partially purified SPDE to in vitro repair reaction mixtures. When the rad12-502 mutant was crossed with the NER rad13-A mutant, the resulting double mutant was much more sensitive to UV radiation than either single mutant, demonstrating that the rad12 gene product functions in a DNA repair pathway distinct from NER. These data directly link SPDE to this alternative excision repair process. We propose that the SPDE-dependent DNA repair pathway is the second DNA excision repair process present in S. pombe.

scholarly journals Archaeal replicative primases can perform translesion DNA synthesis

2015 ◽  
Vol 112 (7) ◽  
pp. E633-E638 ◽  
Author(s):  
Stanislaw K. Jozwiakowski ◽  
Farimah Borazjani Gholami ◽  
Aidan J. Doherty
Keyword(s):  
Dna Synthesis ◽  
Uv Light ◽  
Small Subunit ◽  
Dna Lesions ◽  
Cyclobutane Pyrimidine Dimers ◽  
Translesion Dna Synthesis ◽  
Template Strand ◽  
Pyrimidine Dimers ◽  
Translesion Dna ◽  
Y Family

DNA replicases routinely stall at lesions encountered on the template strand, and translesion DNA synthesis (TLS) is used to rescue progression of stalled replisomes. This process requires specialized polymerases that perform translesion DNA synthesis. Although prokaryotes and eukaryotes possess canonical TLS polymerases (Y-family Pols) capable of traversing blocking DNA lesions, most archaea lack these enzymes. Here, we report that archaeal replicative primases (Pri S, primase small subunit) can also perform TLS. Archaeal Pri S can bypass common oxidative DNA lesions, such as 8-Oxo-2'-deoxyguanosines and UV light-induced DNA damage, faithfully bypassing cyclobutane pyrimidine dimers. Although it is well documented that archaeal replicases specifically arrest at deoxyuracils (dUs) due to recognition and binding to the lesions, a replication restart mechanism has not been identified. Here, we report that Pri S efficiently replicates past dUs, even in the presence of stalled replicase complexes, thus providing a mechanism for maintaining replication bypass of these DNA lesions. Together, these findings establish that some replicative primases, previously considered to be solely involved in priming replication, are also TLS proficient and therefore may play important roles in damage tolerance at replication forks.

scholarly journals The 6-4 photoproduct is the trigger of UV-induced replication blockage and ATR activation

2020 ◽  
Vol 117 (23) ◽  
pp. 12806-12816 ◽  
Author(s):  
Kai-Feng Hung ◽  
Julia M. Sidorova ◽  
Paul Nghiem ◽  
Masaoki Kawasumi
Keyword(s):  
Dna Damage ◽  
Dna Replication ◽  
Cell Cycle Progression ◽  
Dna Lesions ◽  
Multiparameter Flow Cytometry ◽  
Cyclobutane Pyrimidine Dimers ◽  
Pyrimidine Dimers ◽  
Dna Damage Responses ◽  
Atr Activation ◽  
Dna Damage Response Pathway

The most prevalent human carcinogen is sunlight-associated ultraviolet (UV), a physiologic dose of which generates thousands of DNA lesions per cell, mostly of two types: cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproducts (6-4PPs). It has not been possible, in living cells, to precisely characterize the respective contributions of these two lesion types to the signals that regulate cell cycle progression, DNA replication, and cell survival. Here we coupled multiparameter flow cytometry with lesion-specific photolyases that eliminate either CPDs or 6-4PPs and determined their respective contributions to DNA damage responses. Strikingly, only 6-4PP lesions activated the ATR-Chk1 DNA damage response pathway. Mechanistically, 6-4PPs, but not CPDs, impeded DNA replication across the genome as revealed by microfluidic-assisted replication track analysis. Furthermore, single-stranded DNA accumulated preferentially at 6-4PPs during DNA replication, indicating selective and prolonged replication blockage at 6-4PPs. These findings suggest that 6-4PPs, although eightfold fewer in number than CPDs, are the trigger for UV-induced DNA damage responses.

scholarly journals Photoinduced DNA Lesions in Dormant Bacteria. The Peculiar Route Leading to Spore Photoproduct Unraveled by Multiscale Molecular Dynamics

2020 ◽  
Author(s):  
Antonio Francés-Monerris ◽  
Cécilia Hognon ◽  
Thierry Douki ◽  
Antonio Monari
Keyword(s):  
Molecular Dynamics ◽  
Uv Radiation ◽  
Bacterial Species ◽  
Dna Lesions ◽  
Free Energy Barrier ◽  
Structural Factors ◽  
Cyclobutane Pyrimidine Dimers ◽  
Pyrimidine Dimers ◽  
Spore Photoproduct ◽  
Dynamics Simulations

Some bacterial species enter a dormant state in the form of spores to resist to unfavorable external conditions. Spores are resistant to a wide series of stress agents, including UV radiation, and can last for tens to hundreds of years. Due to the suspension of biological functions such as DNA repair, they accumulate DNA damage upon exposure to UV radiation. Differently from active organisms, the most common DNA photoproduct in spores are not cyclobutane pyrimidine dimers, but rather the so-called spore photoproduct. This non-canonical photochemistry results from the dry state of DNA and the binding to small acid soluble proteins that drastically modify the structure and photoreactivity of the nucleic acid. In this contribution, we use multiscale molecular dynamics simulations including extended classical molecular dynamics and QM/MM biased dynamics to elucidate the coupling of electronic and structural factors leading to this photochemical outcome. In particular, we rationalize the well-described impact of the peculiar DNA environment found in spores on the favored formation of the spore photoproduct, given the small free energy barrier found for this path. Meanwhile, the specific organization of spore DNA precludes the photochemical path leading to cyclobutane pyrimidine dimers formation.TOC GRAPHICS

scholarly journals 2,6-diaminopurine promotes repair of DNA lesions under prebiotic conditions

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Rafał Szabla ◽  
Magdalena Zdrowowicz ◽  
Paulina Spisz ◽  
Nicholas J. Green ◽  
Petr Stadlbauer ◽  
...  
Keyword(s):  
Nucleic Acid ◽  
Rna Replication ◽  
Dna Lesions ◽  
Unresolved Issue ◽  
Cyclobutane Pyrimidine Dimers ◽  
Dna Oligomers ◽  
Pyrimidine Dimers ◽  
Prebiotic Environments ◽  
Prebiotic Syntheses ◽  
Rna And Dna

AbstractHigh-yielding and selective prebiotic syntheses of RNA and DNA nucleotides involve UV irradiation to promote the key reaction steps and eradicate biologically irrelevant isomers. While these syntheses were likely enabled by UV-rich prebiotic environment, UV-induced formation of photodamages in polymeric nucleic acids, such as cyclobutane pyrimidine dimers (CPDs), remains the key unresolved issue for the origins of RNA and DNA on Earth. Here, we demonstrate that substitution of adenine with 2,6-diaminopurine enables repair of CPDs with yields reaching 92%. This substantial self-repairing activity originates from excellent electron donating properties of 2,6-diaminopurine in nucleic acid strands. We also show that the deoxyribonucleosides of 2,6-diaminopurine and adenine can be formed under the same prebiotic conditions. Considering that 2,6-diaminopurine was previously shown to increase the rate of nonenzymatic RNA replication, this nucleobase could have played critical roles in the formation of functional and photostable RNA/DNA oligomers in UV-rich prebiotic environments.

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