scholarly journals Multifactorial Resistance ofBacillus subtilisSpores to High-Energy Proton Radiation: Role of Spore Structural Components and the Homologous Recombination and Non-Homologous End Joining DNA Repair Pathways

Astrobiology ◽  
2012 ◽  
Vol 12 (11) ◽  
pp. 1069-1077 ◽  
Author(s):  
Ralf Moeller ◽  
Günther Reitz ◽  
Zuofeng Li ◽  
Stuart Klein ◽  
Wayne L. Nicholson
Keyword(s):  
Dna Repair ◽  
High Energy ◽  
Proton Radiation ◽  
Structural Components ◽  
End Joining ◽  
High Energy Proton ◽  
Energy Proton ◽  
Repair Pathways ◽  
Non Homologous End Joining

scholarly journals ATM antagonizes NHEJ proteins assembly and DNA-ends synapsis at single-ended DNA double strand breaks

2020 ◽  
Vol 48 (17) ◽  
pp. 9710-9723
Author(s):  
Sébastien Britton ◽  
Pauline Chanut ◽  
Christine Delteil ◽  
Nadia Barboule ◽  
Philippe Frit ◽  
...  
Keyword(s):  
Dna Repair ◽  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
End Joining ◽  
Strand Breaks ◽  
Repair Pathways ◽  
Non Homologous End Joining ◽  
Dna Strand ◽  
Dna Ends

Abstract Two DNA repair pathways operate at DNA double strand breaks (DSBs): non-homologous end-joining (NHEJ), that requires two adjacent DNA ends for ligation, and homologous recombination (HR), that resects one DNA strand for invasion of a homologous duplex. Faithful repair of replicative single-ended DSBs (seDSBs) is mediated by HR, due to the lack of a second DNA end for end-joining. ATM stimulates resection at such breaks through multiple mechanisms including CtIP phosphorylation, which also promotes removal of the DNA-ends sensor and NHEJ protein Ku. Here, using a new method for imaging the recruitment of the Ku partner DNA-PKcs at DSBs, we uncover an unanticipated role of ATM in removing DNA-PKcs from seDSBs in human cells. Phosphorylation of DNA-PKcs on the ABCDE cluster is necessary not only for DNA-PKcs clearance but also for the subsequent MRE11/CtIP-dependent release of Ku from these breaks. We propose that at seDSBs, ATM activity is necessary for the release of both Ku and DNA-PKcs components of the NHEJ apparatus, and thereby prevents subsequent aberrant interactions between seDSBs accompanied by DNA-PKcs autophosphorylation and detrimental commitment to Lig4-dependent end-joining.

High-energy proton radiation damage experiment on a hybrid CMOS detector

2020 ◽  
Vol 6 (01) ◽  
pp. 1
Author(s):  
Evan Bray ◽  
Abraham D. Falcone ◽  
Mitchell Wages ◽  
David N. Burrows ◽  
Carl R. Brune ◽  
...  
Keyword(s):  
Radiation Damage ◽  
High Energy ◽  
Proton Radiation ◽  
High Energy Proton ◽  
Energy Proton ◽  
Hybrid Cmos

Comparison of High Energy Proton Radiation Damages on AlGaAs/GaAs and Si Solar Cells

1982 ◽  
Vol 21 (S2) ◽  
pp. 27 ◽  
Author(s):  
Susumu Yoshida ◽  
Kotaro Mitsui ◽  
Takao Oda ◽  
Yoshinory Yukimoto
Keyword(s):  
Solar Cells ◽  
High Energy ◽  
Proton Radiation ◽  
High Energy Proton ◽  
Si Solar Cells ◽  
Energy Proton ◽  
Radiation Damages

Low Energy Proton Radiation Impact on 4H-SiC nMOSFET Gate Oxide Stability

2014 ◽  
Vol 778-780 ◽  
pp. 525-528 ◽  
Author(s):  
Matthieu Florentin ◽  
Mihaela Alexandru ◽  
Aurore Constant ◽  
Bernd Schmidt ◽  
José Millan ◽  
...  
Keyword(s):  
Oxide Layer ◽  
Proton Irradiation ◽  
Electrical Response ◽  
Gate Oxide ◽  
High Energy ◽  
Low Energy ◽  
Electrical Characteristics ◽  
Proton Radiation ◽  
High Energy Proton ◽  
Energy Proton

The 4H-SiC MOSFET electrical response to 180 keV proton radiations at three different fluences has been evaluated. For a certain dose, the devices show an apparent improvement of their electrical characteristics likely due to the N and/or H atoms diffusion inside the oxide layer. This work complete our previous studies on high energy proton irradiation, showing that the 4H-SiC MOSFET is also robust to the low energy proton radiation, when the proton implanted range is located near the MOS interface.

scholarly journals Genome Instability and Pressure on Non-Homologous end Joining drives Chemotherapy Resistance via a DNA Repair Crisis Switch in Triple Negative Breast Cancer.

2020 ◽  
Author(s):  
Adrian Wiegmans ◽  
Ambber Ward ◽  
Ekaterina Ivanova ◽  
Pascal H G Duijf ◽  
Romy VanOosterhout ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Repair ◽  
Homologous Recombination ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Genome Instability ◽  
Chemotherapy Resistance ◽  
End Joining ◽  
Repair Pathways ◽  
Non Homologous End Joining

Abstract Background: Chemotherapy intensifies pressure on the DNA repair pathways that can lead to deregulation. There is an urgent clinical need to be able to track the emergence of chemotherapy resistance and tailor patient staging appropriately. This is especially evident in the triple negative breast cancer (TNBC) subtype, of which standard of care is chemotherapy with tumours displaying high levels of inherent genome instability. TNBC has an overall poor prognosis for survival. There have been numerous studies into single agent chemoresistance but to date no study has elucidated in detail the roles of the key DNA repair components in resistance associated with the frontline clinical combination of anthracyclines and taxanes together. Methods: In this study, we hypothesized that the emergence of chemotherapy resistance is driven by changes in functional signaling in the DNA repair pathways. We identified the importance of the DNA repair pathways in chemoresistant clinical samples and characterized the emergence of chemoresistance in TNBC cell lines. We utilized classical DNA repair assays and specific targeting of key DNA repair proteins to elucidate a new mechanism for adaptation to the combination of doxorubicin and docetaxel. Results: We identified that consistent pressure on the non-homologous end joining pathway in the presence of genome instability causes failure of the key kinase DNA-PK, loss of p53 and compensation by p73. In-turn a switch to reliance on the homologous recombination pathway and RAD51 recombinase occurs to repair residual double strand DNA breaks. Conclusions: We demonstrate that RAD51 is an actionable target for resensitization to chemotherapy in resistant cells with a matched gene expression profile of resistance highlighted by homologous recombination.

scholarly journals Recent Perspectives in Radiation-Mediated DNA Damage and Repair: Role of NHEJ and Alternative Pathways

2021 ◽  
Author(s):  
Ajay Kumar Sharma ◽  
Priyanka Shaw ◽  
Aman Kalonia ◽  
M.H. Yashavarddhan ◽  
Pankaj Chaudhary ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Double Strand Breaks ◽  
Single Strand ◽  
End Joining ◽  
Strand Breaks ◽  
Single Strand Annealing ◽  
Repair Pathways ◽  
Non Homologous End Joining ◽  
Alternative Nhej

Radiation is one of the causative agents for the induction of DNA damage in biological systems. There is various possibility of radiation exposure that might be natural, man-made, intentional, or non-intentional. Published literature indicates that radiation mediated cell death is primarily due to DNA damage that could be a single-strand break, double-strand breaks, base modification, DNA protein cross-links. The double-strand breaks are lethal damage due to the breakage of both strands of DNA. Mammalian cells are equipped with strong DNA repair pathways that cover all types of DNA damage. One of the predominant pathways that operate DNA repair is a non-homologous end-joining pathway (NHEJ) that has various integrated molecules that sense, detect, mediate, and repair the double-strand breaks. Even after a well-coordinated mechanism, there is a strong possibility of mutation due to the flexible nature in joining the DNA strands. There are alternatives to NHEJ pathways that can repair DNA damage. These pathways are alternative NHEJ pathways and single-strand annealing pathways that also displayed a role in DNA repair. These pathways are not studied extensively, and many reports are showing the relevance of these pathways in human diseases. The chapter will very briefly cover the radiation, DNA repair, and Alternative repair pathways in the mammalian system. The chapter will help the readers to understand the basic and applied knowledge of radiation mediated DNA damage and its repair in the context of extensively studied NHEJ pathways and unexplored alternative NHEJ pathways.

scholarly journals Approaches to Enhance Precise CRISPR/Cas9-Mediated Genome Editing

2021 ◽  
Vol 22 (16) ◽  
pp. 8571
Author(s):  
Christopher E. Denes ◽  
Alexander J. Cole ◽  
Yagiz Alp Aksoy ◽  
Geng Li ◽  
G. Gregory Neely ◽  
...  
Keyword(s):  
Dna Repair ◽  
Genome Editing ◽  
Nuclear Dna ◽  
Great Promise ◽  
End Joining ◽  
Strand Breaks ◽  
Homology Directed Repair ◽  
Repair Pathways ◽  
Non Homologous End Joining ◽  
Small Molecule Modulators

Modification of the human genome has immense potential for preventing or treating disease. Modern genome editing techniques based on CRISPR/Cas9 show great promise for altering disease-relevant genes. The efficacy of precision editing at CRISPR/Cas9-induced double-strand breaks is dependent on the relative activities of nuclear DNA repair pathways, including the homology-directed repair and error-prone non-homologous end-joining pathways. The competition between multiple DNA repair pathways generates mosaic and/or therapeutically undesirable editing outcomes. Importantly, genetic models have validated key DNA repair pathways as druggable targets for increasing editing efficacy. In this review, we highlight approaches that can be used to achieve the desired genome modification, including the latest progress using small molecule modulators and engineered CRISPR/Cas proteins to enhance precision editing.

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