Chinese hamster cells meet DNA repair: an entirely acceptable affair

Thompson, Larry H.

doi:10.1002/(sici)1521-1878(199807)20:7<589::aid-bies11>3.0.co;2-w

Cited by 21 publications

(6 citation statements)

References 68 publications

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“…In metazoan cells, several DNA-repair mechanisms such as nucleotide excision repair or base excision repair have been developed to deal with different DNA lesions caused by extrinsic or intrinsic assaults (Lindahl and Wood, 1999). During the 1960s and 70s, a series of DNA-repair mutants in Chinese Hamster Ovary (CHO) cells were isolated by Thompson's lab, which have greatly helped studies of DNA-repair pathways (Thompson, 1998b). For example, a UV-sensitive CHO cell line, UV41, was identified as a mutant of nucleotide excision repair and a human ERCC4 gene, encoding a human nucleotide excision repair protein, can correct the defect of UV41 cells (Thompson et al, 1981;Brookman et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

c-Myc degradation induced by DNA damage results in apoptosis of CHO cells

Jiang

Yang

et al. 2003

Oncogene

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Although tripchlorolide (TC), a compound purified from a Chinese herb Tripterygium Wilfordii Hook, has been demonstrated to be a potent antitumor agent, its mechanisms of action are unknown. The present study shows that TC induces apoptosis of Chinese Hamster Ovary (CHO) cells. Most strikingly, TC was particularly potent in inducing apoptosis of the UV41 mutant CHO cells, which are deficient in the ERCC4 gene encoding a nucleotide excision repair protein. TC caused a higher level of DNA damage in UV41 cells than those in the wildtype CHO cells or EM9 cells, which are deficient in single-strand break repair. These results provided a critical link between apoptotic hypersensitivity and DNA damage in defective nucleotide excision repair pathway of UV41 cells by TC treatment. Further analysis showed that degradation of the c-Myc protein in TC-treated UV41 cells was much stronger than those in the wild-type CHOAA8 and the EM9. A proteasome inhibitor, MG132, reduced both the degradation of c-Myc and apoptosis in TC-treated UV41 cells. Expression of exogenous c-Myc also inhibited apoptosis of TC-treated UV41 cells. These results indicate that c-Myc degradation induced by DNA damage in the presence of TC contributes to induction of apoptosis of UV41 cells.

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Section: Introductionmentioning

confidence: 99%

c-Myc degradation induced by DNA damage results in apoptosis of CHO cells

Jiang

Yang

et al. 2003

Oncogene

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“…6). Only a small amount of SSB was induced directly by UVC-exposure in CHO cell lines (repair-proficient cell line AA8; excision repair-deficient cell line UV5 [29]) irrespective of their repair capacity. In both strains only few free DNA ends accumulate immediately after irradiation up to 60 J/m Ϫ2 .…”

Section: Discussionmentioning

confidence: 99%

“…With the FADU technique it is possible to detect UVC-induced primary SSB and the occurrence of secondary SSB caused by incision enzymes during excision repair. Induction of overall DNA strand breaks after UVC-exposure was measured in repair-proficient CHO cells (cell line AA8) and in CHO cells deficient in the early steps of nucleotide excision repair (cell line UV5, [29]) by the FADU method. DNA induction and repair can be described by purely linear doseeffect curves (Fig.…”

Section: Repair-induced Secondary Dna Strand Breaks After Uvc-exposurementioning

confidence: 99%

Fluorometric Analysis of DNA Unwinding (FADU) as a Method for Detecting Repair-induced DNA Strand Breaks in UV-irradiated Mammalian Cells¶

Baumstark‐Khan

Hentschel²,

Nikandrova

et al. 2000

Photochem Photobiol

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Fluorometric analysis of DNA unwinding (FADU assay) was originally designed to detect X-ray-induced DNA damage in repair-proficient and repair-deficient mammalian cell lines. The method was modified and applied to detect DNA strand breaks in Chinese hamster ovary (CHO) cells exposed to ionizing radiation as well as to UV light. Exposed cells were allowed to repair damaged DNA by incubation for up to 1 h after exposure under standard growth conditions in the presence and in the absence of the DNA synthesis inhibitor aphidicolin. Thereafter, cell lysates were mixed with 0.15 M sodium hydroxide, and DNA unwinding took place at pH 12.1 for 30 min at 20 degrees C. The amount of DNA remaining double-stranded after alkaline reaction was detected by binding to the Hoechst 33258 dye (bisbenzimide) and measuring the fluorescence. After exposure to X-rays DNA strand breaks were observed in all cell lines immediately after exposure with subsequent restitution of high molecular weight DNA during postexposure incubation. In contrast, after UV exposure delayed production of DNA strand break was observed only in cell lines proficient for nucleotide excision repair of DNA photoproducts. Here strand break production was enhanced when the polymerization step was inhibited by adding the repair inhibitor aphidicolin during repair incubation. These results demonstrate that the FADU approach is suitable to distinguish between different DNA lesions (strand breaks versus base alterations) preferentially induced by different environmental radiations (X-rays versus UV) and to distinguish between the different biochemical processes during damage repair (incision versus polymerization and ligation).

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“…Using cell fusion techniques, it was established that seven complementation groups with NER defects exist, XPA through XPG, each representing a different gene defect (De Weerd-Kastelein et al 1972). The availability of the XP cell lines from patients, along with UV-sensitive yeast strains (Prakash and Prakash 2000) and Chinese hamster ovary cell lines (Thompson 1998), made it possible to clone the NER genes over the years (Gillet and Schärer 2006).…”

Section: A Brief History Of Ner Researchmentioning

confidence: 99%

Nucleotide Excision Repair in Eukaryotes

2014

DNA Repair and Mutagenesis

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Nucleotide excision repair (NER) is the main pathway used by mammals to remove bulky DNA lesions such as those formed by UV light, environmental mutagens, and some cancer chemotherapeutic adducts from DNA. Deficiencies in NER are associated with the extremely skin cancer-prone inherited disorder xeroderma pigmentosum. Although the core NER reaction and the factors that execute it have been known for some years, recent studies have led to a much more detailed understanding of the NER mechanism, how NER operates in the context of chromatin, and how it is connected to other cellular processes such as DNA damage signaling and transcription. This review emphasizes biochemical, structural, cell biological, and genetic studies since 2005 that have shed light on many aspects of the NER pathway. N ucleotide excision repair (NER) is the main pathway responsible for the removal of bulky DNA lesions induced by UV irradiation, environmental mutagens, and certain chemotherapeutic agents. The history of the discovery of NER, its association with genetic disorders, mechanistic features, and relationship with other cellular pathways has been extensively reviewed in 2005 in several articles in DNA Repair and Mutagenesis (Friedberg et al. 2005). Here, I will briefly reiterate how the field of NER developed over the past 50 years and then focus on how our knowledge has progressed since 2005.

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Chinese hamster cells meet DNA repair: an entirely acceptable affair

Cited by 21 publications

References 68 publications

c-Myc degradation induced by DNA damage results in apoptosis of CHO cells

c-Myc degradation induced by DNA damage results in apoptosis of CHO cells

Fluorometric Analysis of DNA Unwinding (FADU) as a Method for Detecting Repair-induced DNA Strand Breaks in UV-irradiated Mammalian Cells¶

Nucleotide Excision Repair in Eukaryotes

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