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Molecular Mechanism in DNA Replication and Repair

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biophysics".

Deadline for manuscript submissions: 20 April 2025 | Viewed by 5997

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Institute of Health Sciences, The John Paul II Catholic University of Lublin, Kostantynów 1 H Str., 20-708 Lublin, Poland
Interests: cancer; genomics; molecular biology; health sciences

Special Issue Information

Dear Colleagues,

DNA replication, i.e., making a copy of a cell’s DNA, is a process in which approximately 3 billion base pairs of DNA in the genome must be properly copied when any of the cells divide. DNA replication is semiconservative, which means that each strand in the DNA double helix is a template for the synthesis of a complementary strand. Cells copy their DNA in a fast way, and they use multiple enzymes and proteins in this process, including DNA polymerase, DNA primase, DNA helicase, DNA ligase, and topoisomerase. DNA polymerase could make mistakes while adding nucleotides. Most of the mistakes are corrected during replication, but when it is not employed, the mismatch repair mechanism is implemented, which replaces the incorrect bases with the proper ones. Another type of repair is nucleotide excision repair, which removes incorrect bases along with a few bases on the 3′ and 5′ ends and replaces them by copying the template using DNA polymerase. Most of the mistakes are corrected; uncorrected bases result in mutations, which may cause multiple consequences, such as cancer.

This Special Issue of IJMS is dedicated to understanding and expanding the knowledge of molecular and cellular mechanisms of DNA replication and repair. This Special Issue is supervised by Dr. Ryszard Maciejewski and assisted by our Topical Advisory Panel Member, Dr. Julita Machlowska (Medical University of Lublin). We would like to create a platform for multiple research projects and publications on different aspects of DNA replication and repair mechanisms, which might be significant in terms of novel disease therapies.

Prof. Dr. Ryszard Maciejewski
Guest Editor

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Keywords

  • DNA replication
  • genome stability
  • DNA repair mechanisms
  • mismatch repair mechanism
  • nucleotide excision repair
  • cancer risk

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Published Papers (3 papers)

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Research

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17 pages, 2318 KiB  
Article
Bypass of Methoxyamine-Adducted Abasic Sites by Eukaryotic Translesion DNA Polymerases
by Anna V. Yudkina, Anna A. Novikova, Anastasia D. Stolyarenko, Alena V. Makarova and Dmitry O. Zharkov
Int. J. Mol. Sci. 2025, 26(2), 642; https://doi.org/10.3390/ijms26020642 - 14 Jan 2025
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Abstract
The apurinic/apyrimidinic site (AP site) is a highly mutagenic and cytotoxic DNA lesion. Normally, AP sites are removed from DNA by base excision repair (BER). Methoxyamine (MOX), a BER inhibitor currently under clinical trials as a tumor sensitizer, forms adducts with AP sites [...] Read more.
The apurinic/apyrimidinic site (AP site) is a highly mutagenic and cytotoxic DNA lesion. Normally, AP sites are removed from DNA by base excision repair (BER). Methoxyamine (MOX), a BER inhibitor currently under clinical trials as a tumor sensitizer, forms adducts with AP sites (AP-MOX) resistant to the key BER enzyme, AP endonuclease. As AP-MOX remains unrepaired, translesion DNA synthesis is expected to be the main mechanism of cellular response to this lesion. However, the mutagenic potential of AP-MOX is still unclear. Here, we compare the blocking and mutagenic properties of AP-MOX and the natural AP site for major eukaryotic DNA polymerases involved in translesion synthesis: DNA polymerases η, ι, ζ, Rev1, and primase–polymerase PrimPol. The miscoding properties of both abasic lesions remained mostly the same for each studied enzyme. In contrast, the blocking properties of AP-MOX compared to the AP site were DNA polymerase specific. Pol η and PrimPol bypassed both lesions with the same efficiency. The bypass of AP-MOX by Pol ι was 15-fold lower than that of the AP site. On the contrary, Rev1 bypassed AP-MOX 5-fold better than the AP site. Together, our data suggest that Rev1 is best suited to support synthesis across AP-MOX in human cells. Full article
(This article belongs to the Special Issue Molecular Mechanism in DNA Replication and Repair)
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22 pages, 3574 KiB  
Article
Position-Dependent Effects of AP Sites Within an hTERT Promoter G-Quadruplex Scaffold on Quadruplex Stability and Repair Activity of the APE1 Enzyme
by Viktoriia Yu. Savitskaya, Kirill A. Novoselov, Nina G. Dolinnaya, Mayya V. Monakhova, Viktoriia G. Snyga, Evgeniia A. Diatlova, Elizaveta S. Peskovatskova, Victor M. Golyshev, Mariia I. Kitaeva, Daria A. Eroshenko, Maria I. Zvereva, Dmitry O. Zharkov and Elena A. Kubareva
Int. J. Mol. Sci. 2025, 26(1), 337; https://doi.org/10.3390/ijms26010337 - 2 Jan 2025
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Abstract
Apurinic/apyrimidinic (AP) sites are endogenous DNA lesions widespread in human cells. Having no nucleobases, they are noncoding and promutagenic. AP site repair is generally initiated through strand incision by AP endonuclease 1 (APE1). Although AP sites’ repair in regular B-DNA has been studied [...] Read more.
Apurinic/apyrimidinic (AP) sites are endogenous DNA lesions widespread in human cells. Having no nucleobases, they are noncoding and promutagenic. AP site repair is generally initiated through strand incision by AP endonuclease 1 (APE1). Although AP sites’ repair in regular B-DNA has been studied extensively, their processing in G-quadruplexes (G4s) has received much less attention. Here, we used the hTERT promoter region that is capable of forming three stacked parallel G4s to understand how AP sites can influence higher-order quadruplex folding and stability and how a G4 affects the efficiency of human APE1-mediated AP site processing. We designed a series of synthetic single- and double-stranded DNA constructs of varying lengths containing a stable AP site analog in both G- and C-rich strands at positions corresponding to somatic driver mutations. Using circular dichroism, we studied the effect of the AP site on hTERT G4 structure and stability. Bio-layer interferometry and gel-based approaches were employed to characterize APE1 binding to the designed DNA substrates and AP site processing. It was shown that (i) an AP site leads to G4 destabilization, which depends on the lesion location in the G4 scaffold; (ii) APE1 binds tightly to hTERT G4 structure but exhibits greatly reduced cleavage activity at AP sites embedded in the quadruplex; and (iii) a clear correlation was revealed between AP site-induced hTERT G4 destabilization and APE1 activity. We can hypothesize that reduced repair of AP sites in the hTERT G4 is one of the reasons for the high mutation rate in this promoter region. Full article
(This article belongs to the Special Issue Molecular Mechanism in DNA Replication and Repair)
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Review

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28 pages, 1968 KiB  
Review
The Influence of Circadian Rhythms on DNA Damage Repair in Skin Photoaging
by Zhi Su, Qianhua Hu, Xiang Li, Zirun Wang and Ying Xie
Int. J. Mol. Sci. 2024, 25(20), 10926; https://doi.org/10.3390/ijms252010926 - 11 Oct 2024
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Abstract
Circadian rhythms, the internal timekeeping systems governing physiological processes, significantly influence skin health, particularly in response to ultraviolet radiation (UVR). Disruptions in circadian rhythms can exacerbate UVR-induced skin damage and increase the risk of skin aging and cancer. This review explores how circadian [...] Read more.
Circadian rhythms, the internal timekeeping systems governing physiological processes, significantly influence skin health, particularly in response to ultraviolet radiation (UVR). Disruptions in circadian rhythms can exacerbate UVR-induced skin damage and increase the risk of skin aging and cancer. This review explores how circadian rhythms affect various aspects of skin physiology and pathology, with a special focus on DNA repair. Circadian regulation ensures optimal DNA repair following UVR-induced damage, reducing mutation accumulation, and enhancing genomic stability. The circadian control over cell proliferation and apoptosis further contributes to skin regeneration and response to UVR. Oxidative stress management is another critical area where circadian rhythms exert influence. Key circadian genes like brain and muscle ARNT-like 1 (BMAL1) and circadian locomotor output cycles kaput (CLOCK) modulate the activity of antioxidant enzymes and signaling pathways to protect cells from oxidative stress. Circadian rhythms also affect inflammatory and immune responses by modulating the inflammatory response and the activity of Langerhans cells and other immune cells in the skin. In summary, circadian rhythms form a complex defense network that manages UVR-induced damage through the precise regulation of DNA damage repair, cell proliferation, apoptosis, inflammatory response, oxidative stress, and hormonal signaling. Understanding these mechanisms provides insights into developing targeted skin protection and improving skin cancer prevention. Full article
(This article belongs to the Special Issue Molecular Mechanism in DNA Replication and Repair)
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