scholarly journals Repair of individual DNA strands in the hamster dihydrofolate reductase gene after treatment with ultraviolet light, alkylating agents, and cisplatin.

1993 ◽  
Vol 268 (3) ◽  
pp. 1650-1657
Author(s):  
A. May ◽  
R.S. Nairn ◽  
D.S. Okumoto ◽  
K. Wassermann ◽  
T. Stevnsner ◽  
...  
Keyword(s):  
Ultraviolet Light ◽  
Dihydrofolate Reductase ◽  
Alkylating Agents ◽  
Reductase Gene ◽  
Dna Strands

scholarly journals Identification of Primary Initiation Sites for DNA Replication in the Hamster Dihydrofolate Reductase Gene Initiation Zone

1998 ◽  
Vol 18 (6) ◽  
pp. 3266-3277 ◽  
Author(s):  
Takehiko Kobayashi ◽  
Theo Rein ◽  
Melvin L. DePamphilis
Keyword(s):  
Dihydrofolate Reductase ◽  
Relative Number ◽  
Replication Origins ◽  
Two Dimensional Gel Electrophoresis ◽  
Initiation Zone ◽  
Reductase Gene ◽  
Dna Strands ◽  
Early Replication ◽  
Multiple Replication

ABSTRACT Mammalian replication origins appear paradoxical. While some studies conclude that initiation occurs bidirectionally from specific loci, others conclude that initiation occurs at many sites distributed throughout large DNA regions. To clarify this issue, the relative number of early replication bubbles was determined at 26 sites in a 110-kb locus containing the dihydrofolate reductase (DHFR)-encoding gene in CHO cells; 19 sites were located within an 11-kb sequence containing ori-β. The ratio of ∼0.8-kb nascent DNA strands to nonreplicated DNA at each site was quantified by competitive PCR. Nascent DNA was defined either as DNA that was labeled by incorporation of bromodeoxyuridine in vivo or as RNA-primed DNA that was resistant to λ-exonuclease. Two primary initiation sites were identified within the 12-kb region, where two-dimensional gel electrophoresis previously detected a high frequency of replication bubbles. A sharp peak of nascent DNA occurred at the ori-β origin of bidirectional replication where initiation events were 12 times more frequent than at distal sequences. A second peak occurred 5 kb downstream at a previously unrecognized origin (ori-β′). Thus, the DHFR gene initiation zone contains at least three primary initiation sites (ori-β, ori-β′, and ori-γ), suggesting that initiation zones in mammals, like those in fission yeast, consist of multiple replication origins.

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.

The Effects of Dihydrofolate Reductase Gene on The Development of Pharyngeal Arches*

2010 ◽  
Vol 37 (2) ◽  
pp. 145-153 ◽  
Author(s):  
Shu-Na SUN ◽  
Yong-Hao GUI ◽  
Qiu JIANG ◽  
Lin-Xi QIAN ◽  
Hou-Yan SONG
Keyword(s):  
Dihydrofolate Reductase ◽  
Pharyngeal Arches ◽  
Reductase Gene

scholarly journals Novel DNA rearrangements are associated with dihydrofolate reductase gene amplification.

1984 ◽  
Vol 259 (14) ◽  
pp. 9127-9140
Author(s):  
N A Federspiel ◽  
S M Beverley ◽  
J W Schilling ◽  
R T Schimke
Keyword(s):  
Gene Amplification ◽  
Dihydrofolate Reductase ◽  
Dna Rearrangements ◽  
Reductase Gene

scholarly journals Molecular Basis of In Vivo Resistance to Sulfadoxine-Pyrimethamine in African Adult Patients Infected withPlasmodium falciparum Malaria Parasites

1998 ◽  
Vol 42 (7) ◽  
pp. 1811-1814 ◽  
Author(s):  
Leonardo K. Basco ◽  
Rachida Tahar ◽  
Pascal Ringwald
Keyword(s):  
Dihydrofolate Reductase ◽  
Point Mutations ◽  
Gene Mutations ◽  
Adult Patients ◽  
Wild Type ◽  
Dihydropteroate Synthase ◽  
Reductase Gene ◽  
Parasite Populations

ABSTRACT In vitro sulfadoxine and pyrimethamine resistance has been associated with point mutations in the dihydropteroate synthase and dihydrofolate reductase domains, respectively, but the in vivo relevance of these point mutations has not been well established. To analyze the correlation between genotype and phenotype, 10 Cameroonian adult patients were treated with sulfadoxine-pyrimethamine and followed up for 28 days. After losses to follow-up (n = 1) or elimination of DNA samples due to mixed parasite populations with pyrimethamine-sensitive and pyrimethamine-resistant profiles (n = 3), parasite genomic DNA from day 0 blood samples of six patients were analyzed by DNA sequencing. Three patients who were cured had isolates characterized by a wild-type or mutant dihydrofolate reductase gene (with one or two mutations) and a wild-type dihydropteroate synthase gene. Three other patients who failed to respond to sulfadoxine-pyrimethamine treatment carried isolates with triple dihydrofolate reductase gene mutations and either a wild-type or a mutant dihydropteroate synthase gene. Three dihydrofolate reductase gene codons (51, 59, and 108) may be reliable genetic markers that can accurately predict the clinical outcome of sulfadoxine-pyrimethamine treatment in Africa.

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