Pre-UV-Treatment of Cells Results in Enhanced Host Cell Reactivation of a UV Damaged Reporter Gene in CHO-AA8 Chinese Hamster Ovary Cells but Not in Transcription-Coupled Repair Deficient CHO-UV61 Cells

2004 ◽  
Vol 24 (6) ◽  
pp. 559-576 ◽  
Author(s):  
Lili Liu ◽  
Andrew J. Rainbow
Keyword(s):  
Host Cell ◽  
Reporter Gene ◽  
Chinese Hamster Ovary ◽  
Excision Repair ◽  
Chinese Hamster Ovary Cells ◽  
Chinese Hamster ◽  
Ovary Cells ◽  
Cell Reactivation ◽  
Host Cell Reactivation ◽  
Transcription Coupled Repair

We have used a non-replicating recombinant adenovirus, Ad5MCMVlacZ, which expresses the β-galactosidase reporter gene, to examine both constitutive and inducible repair of UV-damaged DNA in repair proficient CHO-AA8 Chinese hamster ovary cells and in mutant CHO-UV61 cells which are deficient in the transcription-coupled repair (TCR) pathway of nucleotide excision repair. Host cell reactivation (HCR) of β-galactosidase activity for UV-irradiated Ad5MCMVlacZ was significantly reduced in non-irradiated CHO-UV61 cells compared to that in non-irradiated CHO-AA8 cells suggesting that repair in the transcribed strand of the UV-damaged reporter gene in untreated cells utilizes TCR. Prior UV-irradiation of cells with low UV fluences resulted in a transient enhancement of HCR for expression of the UV-damaged reporter gene in CHO-AA8 cells but not in TCR deficient CHO-UV61 cells. These results suggest the presence of an inducible DNA pathway in CHO cells that results from an enhancement of TCR or a mechanism that involves the TCR pathway.

scholarly journals Survival, mutagenesis, and host cell reactivation in a Chinese hamster ovary cell ERCC1 knock-out mutant

Mutagenesis ◽  
1997 ◽  
Vol 12 (4) ◽  
pp. 277-283 ◽  
Author(s):  
Rhonda L. Rolig ◽  
Susan K. Layher ◽  
Barbara Santi ◽  
Gerald M. Adair ◽  
Feng Gu ◽  
...  
Keyword(s):  
Host Cell ◽  
Chinese Hamster Ovary Cell ◽  
Chinese Hamster Ovary ◽  
Chinese Hamster ◽  
Ovary Cell ◽  
Knock Out ◽  
Cell Reactivation ◽  
Host Cell Reactivation

DNA Degradation and Excision Repair in γ-Irradiated Chinese Hamster Ovary Cells

1973 ◽  
Vol 245 (147) ◽  
pp. 230-232 ◽  
Author(s):  
M. R. MATTERN ◽  
P. V. HARIHARAN ◽  
B. E. DUNLAP ◽  
P. A. CERUTTI
Keyword(s):  
Chinese Hamster Ovary ◽  
Excision Repair ◽  
Chinese Hamster Ovary Cells ◽  
Chinese Hamster ◽  
Dna Degradation ◽  
Ovary Cells

scholarly journals Functional nucleotide excision repair is required for the preferential removal of N-ethylpurines from the transcribed strand of the dihydrofolate reductase gene of Chinese hamster ovary cells.

1997 ◽  
Vol 17 (2) ◽  
pp. 564-570 ◽  
Author(s):  
A Sitaram ◽  
G Plitas ◽  
W Wang ◽  
D A Scicchitano
Keyword(s):  
Nucleotide Excision Repair ◽  
Dihydrofolate Reductase ◽  
Chinese Hamster Ovary ◽  
Excision Repair ◽  
Chinese Hamster Ovary Cells ◽  
Alkylating Agents ◽  
Chinese Hamster ◽  
Ovary Cells ◽  
Reductase Gene ◽  
Nucleotide Excision

Transcription-coupled repair of DNA adducts is an essential factor that must be considered when one is elucidating biological endpoints resulting from exposure to genotoxic agents. Alkylating agents comprise one group of chemical compounds which modify DNA by reacting with oxygen and nitrogen atoms in the bases of the double helix. To discern the role of transcription-coupled DNA repair of N-ethylpurines present in discrete genetic domains, Chinese hamster ovary cells were exposed to N-ethyl-N-nitrosourea, and the clearance of the damage from the dihydrofolate reductase gene was investigated. The results indicate that N-ethylpurines were removed from the dihydrofolate reductase gene of nucleotide excision repair-proficient Chinese hamster ovary cells; furthermore, when repair rates in the individual strands were determined, a statistically significant bias in the removal of ethyl-induced, alkali-labile sites was observed, with clearance occurring 30% faster from the transcribed strand than from its nontranscribed counterpart at early times after exposure. In contrast, removal of N-ethylpurines was observed in the dihydrofolate reductase locus in cells that lacked nucleotide excision repair, but both strands were repaired at the same rate, indicating that transcription-coupled clearance of these lesions requires the presence of active nucleotide excision repair.

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