CDC42 Gtpase Activation Affects Hela Cell DNA Repair and Proliferation Following UV Radiation-Induced Genotoxic Stress

2015 ◽  
Vol 116 (9) ◽  
pp. 2086-2097 ◽  
Author(s):  
Liv G. Ascer ◽  
Yuli T. Magalhaes ◽  
Gisele Espinha ◽  
Juliana H. Osaki ◽  
Renan C. Souza ◽  
...  
Keyword(s):  
Dna Repair ◽  
Hela Cell ◽  
Uv Radiation ◽  
Genotoxic Stress ◽  
Radiation Induced ◽  
Gtpase Activation

scholarly journals Excision repair of UV radiation-induced DNA damage in Caenorhabditis elegans.

Genetics ◽  
1989 ◽  
Vol 122 (2) ◽  
pp. 379-385 ◽  
Author(s):  
P S Hartman ◽  
J Hevelone ◽  
V Dwarakanath ◽  
D L Mitchell
Keyword(s):  
Dna Repair ◽  
Uv Radiation ◽  
Excision Repair ◽  
Radiation Sensitivity ◽  
Developmentally Regulated ◽  
Repair Capacity ◽  
C Elegans ◽  
Cyclobutane Dimers ◽  
Radiation Induced ◽  
Dna Photoproducts

Abstract Radioimmunoassays were used to monitor the removal of antibody-binding sites associated with the two major UV radiation-induced DNA photoproducts [cyclobutane dimers and (6-4) photoproducts]. Unlike with cultured human cells, where (6-4) photoproducts are removed more rapidly than cyclobutane dimers, the kinetics of repair were similar for both lesions. Repair capacity in wild type diminished throughout development. The radioimmunoassays were also employed to confirm the absence of photoreactivation in C. elegans. In addition, three radiation-sensitive mutants (rad-1, rad-2, rad-7) displayed normal repair capacities. An excision defect was much more pronounced in larvae than embryos in the fourth mutant tested (rad-3). This correlates with the hypersensitivity pattern of this mutant and suggests that DNA repair may be developmentally regulated in C. elegans. The mechanism of DNA repair in C. elegans as well as the relationship between the repair of specific photoproducts and UV radiation sensitivity during development are discussed.

scholarly journals Prevention of UV radiation–induced immunosuppression by IL-12 is dependent on DNA repair

2005 ◽  
Vol 201 (2) ◽  
pp. 173-179 ◽  
Author(s):  
Agatha Schwarz ◽  
Akira Maeda ◽  
Kerstin Kernebeck ◽  
Harry van Steeg ◽  
Stefan Beissert ◽  
...  
Keyword(s):  
T Cells ◽  
Dna Repair ◽  
Regulatory T Cells ◽  
Uv Radiation ◽  
Contact Hypersensitivity ◽  
Immune Restoration ◽  
Radiation Induced ◽  
Induced Tolerance ◽  
Deficient Mice ◽  
Solar Ultraviolet

The immunostimulatory cytokine IL-12 is able to antagonize immunosuppression induced by solar/ultraviolet (UV) radiation via yet unknown mechanisms. IL-12 was recently found to induce deoxyribonucleic acid (DNA) repair. UV-induced DNA damage is an important molecular trigger for UV-mediated immunosuppression. Thus, we initiated studies into immune restoration by IL-12 to discern whether its effects are linked to DNA repair. IL-12 prevented both UV-induced suppression of the induction of contact hypersensitivity and the depletion of Langerhans cells, the primary APC of the skin, in wild-type but not in DNA repair-deficient mice. IL-12 did not prevent the development of UV-induced regulatory T cells in DNA repair-deficient mice. In contrast, IL-12 was able to break established UV-induced tolerance and inhibited the activity of regulatory T cells independent of DNA repair. These data identify a new mechanism by which IL-12 can restore immune responses and also demonstrate a link between DNA repair and the prevention of UV-induced immunosuppression by IL-12.

scholarly journals Reconstitution of UV-damaged DNA into chromatin using Xenopus oocyte extracts.

1998 ◽  
Vol 45 (2) ◽  
pp. 595-603
Author(s):  
P Widłak
Keyword(s):  
Dna Repair ◽  
Dna Synthesis ◽  
Uv Radiation ◽  
Plasmid Dna ◽  
Xenopus Oocyte ◽  
Chromatin Assembly ◽  
Radiation Induced ◽  
Damaged Dna

Chromatin was reconstituted in vitro using Xenopus oocyte extracts and plasmid DNA containing UV radiation-induced damage. Damaged DNA was assembled into minichromosomes with an efficiency similar to that of control, non-irradiated DNA. Oocyte extracts were competent to carry out DNA repair, which was elicited by nicking damaged templates followed by DNA synthesis during chromatin assembly. Newly synthesized DNA was efficiently reconstituted into nucleosomes.

scholarly journals Coexistence of SOS-Dependent and SOS-Independent Regulation of DNA Repair Genes in Radiation-Resistant Deinococcus Bacteria

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 924
Author(s):  
Laurence Blanchard ◽  
Arjan de Groot
Keyword(s):  
Dna Repair ◽  
Deinococcus Radiodurans ◽  
Dna Repair Genes ◽  
Lesion Bypass ◽  
Radiation Resistant ◽  
Radiation Induced ◽  
Induced Mutagenesis ◽  
High Doses ◽  
Translesion Polymerases ◽  
Repair Genes

Deinococcus bacteria are extremely resistant to radiation and able to repair a shattered genome in an essentially error-free manner after exposure to high doses of radiation or prolonged desiccation. An efficient, SOS-independent response mechanism to induce various DNA repair genes such as recA is essential for radiation resistance. This pathway, called radiation/desiccation response, is controlled by metallopeptidase IrrE and repressor DdrO that are highly conserved in Deinococcus. Among various Deinococcus species, Deinococcus radiodurans has been studied most extensively. Its genome encodes classical DNA repair proteins for error-free repair but no error-prone translesion DNA polymerases, which may suggest that absence of mutagenic lesion bypass is crucial for error-free repair of massive DNA damage. However, many other radiation-resistant Deinococcus species do possess translesion polymerases, and radiation-induced mutagenesis has been demonstrated. At least dozens of Deinococcus species contain a mutagenesis cassette, and some even two cassettes, encoding error-prone translesion polymerase DnaE2 and two other proteins, ImuY and ImuB-C, that are probable accessory factors required for DnaE2 activity. Expression of this mutagenesis cassette is under control of the SOS regulators RecA and LexA. In this paper, we review both the RecA/LexA-controlled mutagenesis and the IrrE/DdrO-controlled radiation/desiccation response in Deinococcus.

scholarly journals The Large Subunit of Replication Factor C (Rfclp/Cdc44p) Is Required for DNA Replication and DNA Repair in Saccharomyces cerevisiae

Genetics ◽  
1996 ◽  
Vol 142 (1) ◽  
pp. 65-78 ◽  
Author(s):  
Michael A McAlear ◽  
K Michelle Tuffo ◽  
Connie Holm
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Repair ◽  
Dna Replication ◽  
Uv Radiation ◽  
Large Subunit ◽  
Restrictive Temperature ◽  
Replication Factor C ◽  
Replication Factor ◽  
Factor C

We used genetic and biochemical techniques to characterize the phenotypes associated with mutations affecting the large subunit of replication factor C (Cdc44p or Rfc1p) in Saccharomyces cerevisiae. We demonstrate that Cdc44p is required for both DNA replication and DNA repair in vivo. Cold-sensitive cdc44 mutants experience a delay in traversing S phase at the restrictive temperature following alpha factor arrest; although mutant cells eventually accumulate with a G2/M DNA content, they undergo a cell cycle arrest and initiate neither mitosis nor a new round of DNA synthesis. cdc44 mutants also exhibit an elevated level of spontaneous mutation, and they are sensitive both to the DNA damaging agent methylmethane sulfonate and to exposure to UV radiation. After exposure to UV radiation, cdc44 mutants at the restrictive temperature contain higher levels of single-stranded DNA breaks than do wild-type cells. This observation is consistent with the hypothesis that Cdc44p is involved in repairing gaps in the DNA after the excision of damaged bases. Thus, Cdc44p plays an important role in both DNA replication and DNA repair in vivo.

Communication of Radiation-Induced Signals in Vivo between DNA Repair Deficient and Proficient Medaka (Oryzias latipes)

2009 ◽  
Vol 43 (9) ◽  
pp. 3335-3342 ◽  
Author(s):  
C. Mothersill ◽  
R. W. Smith ◽  
T. G. Hinton ◽  
K. Aizawa ◽  
C. B. Seymour
Keyword(s):  
Dna Repair ◽  
Oryzias Latipes ◽  
Radiation Induced

scholarly journals Exploring the multiple roles of guardian of the genome: P53

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Wasim Feroz ◽  
Arwah Mohammad Ali Sheikh
Keyword(s):  
Cell Cycle ◽  
Dna Repair ◽  
Crucial Role ◽  
Cellular Response ◽  
Genotoxic Stress ◽  
Specific Response ◽  
Main Body ◽  
Repair System ◽  
Tumour Suppression

Abstract Background Cells have evolved balanced mechanisms to protect themselves by initiating a specific response to a variety of stress. The TP53 gene, encoding P53 protein, is one of the many widely studied genes in human cells owing to its multifaceted functions and complex dynamics. The tumour-suppressing activity of P53 plays a principal role in the cellular response to stress. The majority of the human cancer cells exhibit the inactivation of the P53 pathway. In this review, we discuss the recent advancements in P53 research with particular focus on the role of P53 in DNA damage responses, apoptosis, autophagy, and cellular metabolism. We also discussed important P53-reactivation strategies that can play a crucial role in cancer therapy and the role of P53 in various diseases. Main body We used electronic databases like PubMed and Google Scholar for literature search. In response to a variety of cellular stress such as genotoxic stress, ischemic stress, oncogenic expression, P53 acts as a sensor, and suppresses tumour development by promoting cell death or permanent inhibition of cell proliferation. It controls several genes that play a role in the arrest of the cell cycle, cellular senescence, DNA repair system, and apoptosis. P53 plays a crucial role in supporting DNA repair by arresting the cell cycle to purchase time for the repair system to restore genome stability. Apoptosis is essential for maintaining tissue homeostasis and tumour suppression. P53 can induce apoptosis in a genetically unstable cell by interacting with many pro-apoptotic and anti-apoptotic factors. Furthermore, P53 can activate autophagy, which also plays a role in tumour suppression. P53 also regulates many metabolic pathways of glucose, lipid, and amino acid metabolism. Thus under mild metabolic stress, P53 contributes to the cell’s ability to adapt to and survive the stress. Conclusion These multiple levels of regulation enable P53 to perform diversified roles in many cell responses. Understanding the complete function of P53 is still a work in progress because of the inherent complexity involved in between P53 and its target proteins. Further research is required to unravel the mystery of this Guardian of the genome “TP53”.

scholarly journals Mechanistic Modelling of DNA Repair and Cellular Survival Following Radiation-Induced DNA Damage

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Stephen J. McMahon ◽  
Jan Schuemann ◽  
Harald Paganetti ◽  
Kevin M. Prise
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Mechanistic Modelling ◽  
Cellular Survival ◽  
Radiation Induced
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