scholarly journals Correction to ‘DNA repair factor XPC is modified by SUMO-1 and ubiquitin following UV irradiation’

2021 ◽  
Author(s):  
Qi-En Wang ◽  
Qianzheng Zhu ◽  
Gulzar Wani ◽  
Mohamed A El-Mahdy ◽  
Jinyou Li ◽  
...  
Keyword(s):  
Dna Repair ◽  
Uv Irradiation ◽  
Repair Factor

scholarly journals Two Sides of the Same Coin: TFIIH Complexes in Transcription and DNA Repair

2010 ◽  
Vol 10 ◽  
pp. 633-643 ◽  
Author(s):  
Alexander Zhovmer ◽  
Valentyn Oksenych ◽  
Frédéric Coin
Keyword(s):  
Dna Repair ◽  
Western Blotting ◽  
Chromatin Immunoprecipitation ◽  
Transcription Initiation ◽  
Dna Lesions ◽  
Dynamic Composition ◽  
The Core ◽  
Repair Factor ◽  
A New Technique ◽  
Two Sides

TFIIH is organized into a seven-subunit core associated with a three-subunit Cdk-activating kinase (CAK) module. TFIIH has roles in both transcription initiation and DNA repair. During the last 15 years, several studies have been conducted to identify the composition of the TFIIH complex involved in DNA repair. Recently, a new technique combining chromatin immunoprecipitation and western blotting resolved the hidden nature of the TFIIH complex participating in DNA repair. Following the recruitment of TFIIH to the damaged site, the CAK module is released from the core TFIIH, and the core subsequently associates with DNA repair factors. The release of the CAK is specifically driven by the recruitment of the DNA repair factor XPA and is required to promote the incision/excision of the damaged DNA. Once the DNA lesions have been repaired, the CAK module returns to the core TFIIH on the chromatin, together with the release of the repair factors. These data highlight the dynamic composition of a fundamental cellular factor that adapts its subunit composition to the cell needs.

scholarly journals The essential DNA polymerases delta and epsilon are involved in repair of UV-damaged DNA in the yeast Saccharomyces cerevisiae.

1999 ◽  
Vol 46 (2) ◽  
pp. 289-298 ◽  
Author(s):  
A Hałas ◽  
Z Policińska ◽  
H Baranowska ◽  
W J Jachymczyk
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Repair ◽  
Uv Irradiation ◽  
Dna Polymerases ◽  
Relative Molecular Mass ◽  
Yeast Saccharomyces Cerevisiae ◽  
Strand Breaks ◽  
Single Strand Breaks ◽  
Mutant Strains ◽  
Cellular Dna

We have studied the ability of yeast DNA polymerases to carry out repair of lesions caused by UV irradiation in Saccharomyces cerevisiae. By the analysis of postirradiation relative molecular mass changes in cellular DNA of different DNA polymerases mutant strains, it was established that mutations in DNA polymerases delta and epsilon showed accumulation of single-strand breaks indicating defective repair. Mutations in other DNA polymerase genes exhibited no defects in DNA repair. Thus, the data obtained suggest that DNA polymerases delta and epsilon are both necessary for DNA replication and for repair of lesions caused by UV irradiation. The results are discussed in the light of current concepts concerning the specificity of DNA polymerases in DNA repair.

Involvement of the cgtA gene function in stimulation of DNA repair in Escherichia coli and Vibrio harveyi

Microbiology ◽  
2003 ◽  
Vol 149 (7) ◽  
pp. 1763-1770 ◽  
Author(s):  
Ryszard Zielke ◽  
Aleksandra Sikora ◽  
Rafał Dutkiewicz ◽  
Grzegorz Wegrzyn ◽  
Agata Czyż
Keyword(s):  
Gene Expression ◽  
Escherichia Coli ◽  
Dna Repair ◽  
Gene Product ◽  
Uv Irradiation ◽  
Vibrio Harveyi ◽  
Bacterial Species ◽  
Wild Type ◽  
E Coli ◽  
Stimulation Of

CgtA is a member of the Obg/Gtp1 subfamily of small GTP-binding proteins. CgtA homologues have been found in various prokaryotic and eukaryotic organisms, ranging from bacteria to humans. Nevertheless, despite the fact that cgtA is an essential gene in most bacterial species, its function in the regulation of cellular processes is largely unknown. Here it has been demonstrated that in two bacterial species, Escherichia coli and Vibrio harveyi, the cgtA gene product enhances survival of cells after UV irradiation. Expression of the cgtA gene was found to be enhanced after UV irradiation of both E. coli and V. harveyi. Moderate overexpression of cgtA resulted in higher UV resistance of E. coli wild-type and dnaQ strains, but not in uvrA, uvrB, umuC and recA mutant hosts. Overexpression of the E. coli recA gene in the V. harveyi cgtA mutant, which is very sensitive to UV light, restored the level of survival of UV-irradiated cells to the levels observed for wild-type bacteria. Moreover, the basal level of the RecA protein was lower in a temperature-sensitive cgtA mutant of E. coli than in the cgtA + strain, and contrary to wild-type bacteria, no significant increase in recA gene expression was observed after UV irradiation of this cgtA mutant. Finally, stimulation of uvrB gene transcription under these conditions was impaired in the V. harveyi cgtA mutant. All these results strongly suggest that the cgtA gene product is involved in DNA repair processes, most probably by stimulation of recA gene expression and resultant activation of RecA-dependent DNA repair pathways.

Study of UV-induced DNA Repair Factor Recruitment: Kinetics and Dynamics

2017 ◽  
pp. 101-105 ◽  
Author(s):  
Sarah Sertic ◽  
Stefania Roma ◽  
Paolo Plevani ◽  
Federico Lazzaro ◽  
Marco Muzi-Falconi
Keyword(s):  
Dna Repair ◽  
Kinetics And Dynamics ◽  
Repair Factor

scholarly journals Functional Characterization of Excision Repair and RecA-Dependent Recombinational DNA Repair in Campylobacter jejuni

2009 ◽  
Vol 191 (12) ◽  
pp. 3785-3793 ◽  
Author(s):  
Esther J. Gaasbeek ◽  
Fimme J. van der Wal ◽  
Jos P. M. van Putten ◽  
Paulo de Boer ◽  
Linda van der Graaf-van Bloois ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Campylobacter Jejuni ◽  
Uv Irradiation ◽  
Excision Repair ◽  
Spontaneous Mutation ◽  
Functional Characterization ◽  
Point Mutations ◽  
Phase Variable ◽  
Repair Mechanisms

ABSTRACT The presence and functionality of DNA repair mechanisms in Campylobacter jejuni are largely unknown. In silico analysis of the complete translated genome of C. jejuni NCTC 11168 suggests the presence of genes involved in methyl-directed mismatch repair (MMR), nucleotide excision repair, base excision repair (BER), and recombinational repair. To assess the functionality of these putative repair mechanisms in C. jejuni, mutS, uvrB, ung, and recA knockout mutants were constructed and analyzed for their ability to repair spontaneous point mutations, UV irradiation-induced DNA damage, and nicked DNA. Inactivation of the different putative DNA repair genes did not alter the spontaneous mutation frequency. Disruption of the UvrB and RecA orthologues, but not the putative MutS or Ung proteins, resulted in a significant reduction in viability after exposure to UV irradiation. Assays performed with uracil-containing plasmid DNA showed that the putative uracil-DNA glycosylase (Ung) protein, important for initiation of the BER pathway, is also functional in C. jejuni. Inactivation of recA also resulted in a loss of natural transformation. Overall, the data indicate that C. jejuni has multiple functional DNA repair systems that may protect against DNA damage and limit the generation of genetic diversity. On the other hand, the apparent absence of a functional MMR pathway may enhance the frequency of on-and-off switching of phase variable genes typical for C. jejuni and may contribute to the genetic heterogeneity of the C. jejuni population.

scholarly journals Erratum: Ubiquitous overexpression of the DNA repair factor dPrp19 reduces DNA damage and extends Drosophila life span

2017 ◽  
Vol 3 (1) ◽  
Author(s):  
Kathrin Garschall ◽  
Hanna Dellago ◽  
Martina Gáliková ◽  
Markus Schosserer ◽  
Thomas Flatt ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Life Span ◽  
Repair Factor

Abstract 4232: GFP imaging of DNA repair after UV irradiation of cancer cells

2012 ◽  
Author(s):  
Yasunori Tome ◽  
Shuya Yano ◽  
Hiroki Maehara ◽  
Elena V. Efimova ◽  
Fuminori Kanaya ◽  
...  
Keyword(s):  
Dna Repair ◽  
Cancer Cells ◽  
Uv Irradiation

scholarly journals Growth Retardation, Early Death, and DNA Repair Defects in Mice Deficient for the Nucleotide Excision Repair Enzyme XPF

2004 ◽  
Vol 24 (3) ◽  
pp. 1200-1205 ◽  
Author(s):  
Ming Tian ◽  
Reiko Shinkura ◽  
Nobuhiko Shinkura ◽  
Frederick W. Alt
Keyword(s):  
Dna Repair ◽  
Nucleotide Excision Repair ◽  
Uv Irradiation ◽  
Excision Repair ◽  
Genetic Defect ◽  
Growth Defect ◽  
Human Genetic Disease ◽  
Nucleotide Excision ◽  
Deficient Mice

ABSTRACT Xeroderma pigmentosum (XP) is a human genetic disease which is caused by defects in nucleotide excision repair. Since this repair pathway is responsible for removing UV irradiation-induced damage to DNA, XP patients are hypersensitive to sunlight and are prone to develop skin cancer. Based on the underlying genetic defect, the disease can be divided into the seven complementation groups XPA through XPG. XPF, in association with ERCC1, constitutes a structure-specific endonuclease that makes an incision 5′ to the photodamage. XPF-ERCC1 has also been implicated in both removal of interstrand DNA cross-links and homology-mediated recombination and in immunoglobulin class switch recombination (CSR). To study the function of XPF in vivo, we inactivated the XPF gene in mice. XPF-deficient mice showed a severe postnatal growth defect and died approximately 3 weeks after birth. Histological examination revealed that the liver of mutant animals contained abnormal cells with enlarged nuclei. Furthermore, embryonic fibroblasts defective in XPF are hypersensitive to UV irradiation and mitomycin C treatment. No defect in CSR was detected, suggesting that the nuclease is dispensable for this recombination process. These phenotypes are identical to those exhibited by the ERCC1-deficient mice, consistent with the functional association of the two proteins. The complex phenotype suggests that XPF-ERCC1 is involved in multiple DNA repair processes.

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