scholarly journals A ubiquitylation site in Cockayne syndrome B required for repair of oxidative DNA damage, but not for transcription-coupled nucleotide excision repair

2016 ◽  
Vol 44 (11) ◽  
pp. 5246-5255 ◽  
Author(s):  
Michael Ranes ◽  
Stefan Boeing ◽  
Yuming Wang ◽  
Franziska Wienholz ◽  
Hervé Menoni ◽  
...  
Keyword(s):  
Dna Damage ◽  
Nucleotide Excision Repair ◽  
Oxidative Dna Damage ◽  
Excision Repair ◽  
Cockayne Syndrome ◽  
Nucleotide Excision

scholarly journals Oxidative DNA Damage and Nucleotide Excision Repair

2013 ◽  
Vol 18 (18) ◽  
pp. 2409-2419 ◽  
Author(s):  
Joost P.M. Melis ◽  
Harry van Steeg ◽  
Mirjam Luijten
Keyword(s):  
Dna Damage ◽  
Nucleotide Excision Repair ◽  
Oxidative Dna Damage ◽  
Excision Repair ◽  
Nucleotide Excision

Genotoxicity of Soluble and Particulate Cadmium Compounds: Impact on Oxidative DNA Damage and Nucleotide Excision Repair

2010 ◽  
Vol 23 (2) ◽  
pp. 432-442 ◽  
Author(s):  
Tanja Schwerdtle ◽  
Franziska Ebert ◽  
Christina Thuy ◽  
Constanze Richter ◽  
Leon H. F. Mullenders ◽  
...  
Keyword(s):  
Dna Damage ◽  
Nucleotide Excision Repair ◽  
Oxidative Dna Damage ◽  
Excision Repair ◽  
Cadmium Compounds ◽  
Nucleotide Excision

Role of nucleotide excision repair proteins in oxidative DNA damage repair: an updating

2011 ◽  
Vol 76 (1) ◽  
pp. 4-15 ◽  
Author(s):  
B. Pascucci ◽  
M. D’Errico ◽  
E. Parlanti ◽  
S. Giovannini ◽  
E. Dogliotti
Keyword(s):  
Dna Damage ◽  
Nucleotide Excision Repair ◽  
Oxidative Dna Damage ◽  
Excision Repair ◽  
Dna Damage Repair ◽  
Damage Repair ◽  
Nucleotide Excision

scholarly journals Different Effects of CSA and CSB Deficiency on Sensitivity to Oxidative DNA Damage

2004 ◽  
Vol 24 (18) ◽  
pp. 7941-7948 ◽  
Author(s):  
Harm de Waard ◽  
Jan de Wit ◽  
Jaan-Olle Andressoo ◽  
Conny T. M. van Oostrom ◽  
Bente Riis ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Damage Response ◽  
Oxidative Dna Damage ◽  
Gamma Ray ◽  
Excision Repair ◽  
Embryonic Stem ◽  
Cockayne Syndrome ◽  
Nucleotide Excision ◽  
Damage Response ◽  
Transcription Coupled Repair

ABSTRACT Mutations in the CSA and CSB genes cause Cockayne syndrome, a rare inherited disorder characterized by UV sensitivity, severe neurological abnormalities, and progeriod symptoms. Both gene products function in the transcription-coupled repair (TCR) subpathway of nucleotide excision repair (NER), providing the cell with a mechanism to remove transcription-blocking lesions from the transcribed strands of actively transcribed genes. Besides a function in TCR of NER lesions, a role of CSB in (transcription-coupled) repair of oxidative DNA damage has been suggested. In this study we used mouse models to compare the effect of a CSA or a CSB defect on oxidative DNA damage sensitivity at the levels of the cell and the intact organism. In contrast to CSB −/− mouse embryonic fibroblasts (MEFs), CSA −/− MEFs are not hypersensitive to gamma-ray or paraquat treatment. Similar results were obtained for keratinocytes. In contrast, both CSB −/− and CSA −/− embryonic stem cells show slight gamma-ray sensitivity. Finally, CSB −/− but not CSA −/− mice fed with food containing di(2-ethylhexyl)phthalate (causing elevated levels of oxidative DNA damage in the liver) show weight reduction. These findings not only uncover a clear difference in oxidative DNA damage sensitivity between CSA- and CSB-deficient cell lines and mice but also show that sensitivity to oxidative DNA damage is not a uniform characteristic of Cockayne syndrome. This difference in the DNA damage response between CSA- and CSB-deficient cells is unexpected, since until now no consistent differences between CSA and CSB patients have been reported. We suggest that the CSA and CSB proteins in part perform separate roles in different DNA damage response pathways.

scholarly journals The role of nucleotide excision repair in protecting embryonic stem cells from genotoxic effects of UV-induced DNA damage

1999 ◽  
Vol 27 (16) ◽  
pp. 3276-3282 ◽  
Author(s):  
P. P. H. Van Sloun ◽  
J. G. Jansen ◽  
G. Weeda ◽  
L. H. F. Mullenders ◽  
A. A. van Zeeland ◽  
...  
Keyword(s):  
Stem Cells ◽  
Dna Damage ◽  
Embryonic Stem Cells ◽  
Nucleotide Excision Repair ◽  
Excision Repair ◽  
Embryonic Stem ◽  
Genotoxic Effects ◽  
Nucleotide Excision

scholarly journals Flipping of alkylated DNA damage bridges base and nucleotide excision repair

Nature ◽  
2009 ◽  
Vol 459 (7248) ◽  
pp. 808-813 ◽  
Author(s):  
Julie L. Tubbs ◽  
Vitaly Latypov ◽  
Sreenivas Kanugula ◽  
Amna Butt ◽  
Manana Melikishvili ◽  
...  
Keyword(s):  
Dna Damage ◽  
Nucleotide Excision Repair ◽  
Excision Repair ◽  
Nucleotide Excision

scholarly journals Nucleotide Excision Repair Protein Rad23 Regulates Cell Virulence Independent of Rad4 in Candida albicans

mSphere ◽  
2020 ◽  
Vol 5 (1) ◽  
Author(s):  
Jia Feng ◽  
Shuangyan Yao ◽  
Yansong Dong ◽  
Jing Hu ◽  
Malcolm Whiteway ◽  
...  
Keyword(s):  
Dna Damage ◽  
Candida Albicans ◽  
Nucleotide Excision Repair ◽  
Dna Damage Response ◽  
Excision Repair ◽  
Content Type ◽  
Virulence Regulation ◽  
Nucleotide Excision ◽  
Damage Response

ABSTRACT In the pathogenic yeast Candida albicans, the DNA damage response contributes to pathogenicity by regulating cell morphology transitions and maintaining survival in response to DNA damage induced by reactive oxygen species (ROS) in host cells. However, the function of nucleotide excision repair (NER) in C. albicans has not been extensively investigated. To better understand the DNA damage response and its role in virulence, we studied the function of the Rad23 nucleotide excision repair protein in detail. The RAD23 deletion strain and overexpression strain both exhibit UV sensitivity, confirming the critical role of RAD23 in the nucleotide excision repair pathway. Genetic interaction assays revealed that the role of RAD23 in the UV response relies on RAD4 but is independent of RAD53, MMS22, and RAD18. RAD4 and RAD23 have similar roles in regulating cell morphogenesis and biofilm formation; however, only RAD23, but not RAD4, plays a negative role in virulence regulation in a mouse model. We found that the RAD23 deletion strain showed decreased survival in a Candida-macrophage interaction assay. Transcriptome sequencing (RNA-seq) and quantitative real-time PCR (qRT-PCR) data further revealed that RAD23, but not RAD4, regulates the transcription of a virulence factor, SUN41, suggesting a unique role of RAD23 in virulence regulation. Taking these observations together, our work reveals that the RAD23-related nucleotide excision pathway plays a critical role in the UV response but may not play a direct role in virulence. The virulence-related role of RAD23 may rely on the regulation of several virulence factors, which may give us further understanding about the linkage between DNA damage repair and virulence regulation in C. albicans. IMPORTANCE Candida albicans remains a significant threat to the lives of immunocompromised people. An understanding of the virulence and infection ability of C. albicans cells in the mammalian host may help with clinical treatment and drug discovery. The DNA damage response pathway is closely related to morphology regulation and virulence, as well as the ability to survive in host cells. In this study, we checked the role of the nucleotide excision repair (NER) pathway, the key repair system that functions to remove a large variety of DNA lesions such as those caused by UV light, but whose function has not been well studied in C. albicans. We found that Rad23, but not Rad4, plays a role in virulence that appears independent of the function of the NER pathway. Our research revealed that the NER pathway represented by Rad4/Rad23 may not play a direct role in virulence but that Rad23 may play a unique role in regulating the transcription of virulence genes that may contribute to the virulence of C. albicans.

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