scholarly journals DNA repair in higher plants; photoreactivation is the major DNA repair pathway in non-proliferating cells while excision repair (nucleotide excision repair and base excision repair) is active in proliferating cells

2004 ◽  
Vol 32 (9) ◽  
pp. 2760-2767 ◽  
Author(s):  
S. Kimura
2000 ◽  
Vol 182 (8) ◽  
pp. 2104-2112 ◽  
Author(s):  
Asli Memisoglu ◽  
Leona Samson

ABSTRACT DNA damage is unavoidable, and organisms across the evolutionary spectrum possess DNA repair pathways that are critical for cell viability and genomic stability. To understand the role of base excision repair (BER) in protecting eukaryotic cells against alkylating agents, we generated Schizosaccharomyces pombe strains mutant for the mag1 3-methyladenine DNA glycosylase gene. We report that S. pombe mag1 mutants have only a slightly increased sensitivity to methylation damage, suggesting that Mag1-initiated BER plays a surprisingly minor role in alkylation resistance in this organism. We go on to show that other DNA repair pathways play a larger role than BER in alkylation resistance. Mutations in genes involved in nucleotide excision repair (rad13) and recombinational repair (rhp51) are much more alkylation sensitive thanmag1 mutants. In addition, S. pombe mutant for the flap endonuclease rad2 gene, whose precise function in DNA repair is unclear, were also more alkylation sensitive thanmag1 mutants. Further, mag1 andrad13 interact synergistically for alkylation resistance, and mag1 and rhp51 display a surprisingly complex genetic interaction. A model for the role of BER in the generation of alkylation-induced DNA strand breaks in S. pombe is discussed.


1984 ◽  
Vol 99 (4) ◽  
pp. 1275-1281 ◽  
Author(s):  
P K Gupta ◽  
M A Sirover

The regulation of DNA repair during serum stimulation of quiescent cells was examined in normal human cells, in fibroblasts from three xeroderma pigmentosum complementation groups (A, C, and D), in xeroderma pigmentosum variant cells, and in ataxia telangiectasia cells. The regulation of nucleotide excision repair was examined by exposing cells to ultraviolet irradiation at discrete intervals after cell stimulation. Similarly, base excision repair was quantitated after exposure to methylmethane sulfonate. WI-38 normal human diploid fibroblasts, xeroderma pigmentosum variant cells, as well as ataxia telangiectasia cells enhanced their capacity for both nucleotide excision repair and for base excision repair prior to their enhancement of DNA synthesis. Further, in each cell strain, the base excision repair enzyme uracil DNA glycosylase was increased prior to the induction of DNA polymerase using the identical cells to quantitate each activity. In contrast, each of the three xeroderma complementation groups that were examined failed to increase their capacity for nucleotide excision repair above basal levels at any interval examined. This result was observed using either unscheduled DNA synthesis in the presence of 10 mM hydroxyurea or using repair replication in the absence of hydroxyurea to quantitate DNA repair. However, each of the three complementation groups normally regulated the enhancement of base excision repair after methylmethane sulfonate exposure and each induced the uracil DNA glycosylase prior to DNA synthesis. These results suggest that there may be a relationship between the sensitivity of xeroderma pigmentosum cells from each complementation group to specific DNA damaging agents and their inability to regulate nucleotide excision repair during cell stimulation.


2021 ◽  
Vol 121 ◽  
pp. 104987
Author(s):  
Fernanda Aragão Felix ◽  
Leorik Pereira da Silva ◽  
Maria Luiza Diniz de Sousa Lopes ◽  
Ana Paula Veras Sobral ◽  
Roseana de Almeida Freitas ◽  
...  

Author(s):  
David A Farnell

Nucleotide excision repair (NER) is a vital DNA repair pathway which acts on a wide range of helix-distorting lesions. The importance of this pathway is highlighted by its functional conservation throughout evolution and by several human diseases, such as xeroderma pigmentosum, which are caused by a defective NER pathway. This review summarizes the NER mechanisms present in all three domains of life: eukaryotes, bacteria, and archaea.


2009 ◽  
Vol 30 (3) ◽  
pp. 408-415 ◽  
Author(s):  
D. Sagan ◽  
R. Muller ◽  
C. Kroger ◽  
A. Hematulin ◽  
S. Mortl ◽  
...  

FEBS Letters ◽  
1999 ◽  
Vol 450 (3) ◽  
pp. 197-204 ◽  
Author(s):  
Hagai Offer ◽  
Roland Wolkowicz ◽  
Devorah Matas ◽  
Sara Blumenstein ◽  
Zvi Livneh ◽  
...  

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