Effect of gamma rays on efficiency of gene transfer in DNA repair-proficient and -deficient cell lines

1988 ◽  
Vol 14 (6) ◽  
pp. 613-621 ◽  
Author(s):  
Jaime S. Rubin
Keyword(s):  
Dna Repair ◽  
Gene Transfer ◽  
Cell Lines ◽  
Gamma Rays ◽  
Deficient Cell

scholarly journals Purine DNA Lesions at Different Oxygen Concentration in DNA Repair-Impaired Human Cells (EUE-siXPA)

Cells ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 1377 ◽  
Author(s):  
Krokidis ◽  
Parlanti ◽  
D’Errico ◽  
Pascucci ◽  
Pino ◽  
...  
Keyword(s):  
Dna Repair ◽  
Cell Lines ◽  
Oxygen Concentration ◽  
Excision Repair ◽  
Cell Types ◽  
Dna Lesions ◽  
Deficient Cell ◽  
Liquid Chromatography Tandem Mass ◽  
Order Of Magnitude

Xeroderma Pigmentosum (XP) is a DNA repair disease characterized by nucleotide excision repair (NER) malfunction, leading to photosensitivity and increased incidence of skin malignancies. The role of XP-A in NER pathways has been well studied while discrepancies associated with ROS levels and the role of radical species between normal and deficient XPA cell lines have been observed. Using liquid chromatography tandem mass spectrometry we have determined the four 5’,8-cyclopurines (cPu) lesions (i.e., 5′R-cdG, 5′S-cdG, 5′R-cdA and 5′S-cdA), 8-oxo-dA and 8-oxo-dG in wt (EUE-pBD650) and XPA-deficient (EUE-siXPA) human embryonic epithelial cell lines, under different oxygen tension (hyperoxic 21%, physioxic 5% and hypoxic 1%). The levels of Fe and Cu were also measured. The main findings of our study were: (i) the total amount of cPu (1.82–2.52 lesions/106 nucleotides) is the same order of magnitude as 8-oxo-Pu (3.10–4.11 lesions/106 nucleotides) in both cell types, (ii) the four cPu levels are similar in hyperoxic and physioxic conditions for both wt and deficient cell lines, whereas 8-oxo-Pu increases in all cases, (iii) both wt and deficient cell lines accumulated high levels of cPu under hypoxic compared to physioxic conditions, whereas the 8-oxo-Pu levels show an opposite trend, (iv) the diastereoisomeric ratios 5′R/5′S are independent of oxygen concentration being 0.29 for cdG and 2.69 for cdA for EUE-pBD650 (wt) and 0.32 for cdG and 2.94 for cdA for EUE-siXPA (deficient), (v) in deficient cell lines Fe levels were significantly higher. The data show for the first time the connection of oxygen concentration in cells with different DNA repair ability and the levels of different DNA lesions highlighting the significance of cPu. Membrane lipidomic data at 21% O2 indicated differences in the fatty acid contents between wild type and deficient cells, envisaging functional effects on membranes associated with the different repair capabilities, to be further investigated.

scholarly journals Comparison of cellular lethality in DNA repair-proficient or -deficient cell lines resulting from exposure to 70 MeV/n protons or 290 MeV/n carbon ions

2012 ◽  
Vol 28 (5) ◽  
pp. 1591-1596 ◽  
Author(s):  
STEFAN C. GENET ◽  
JUNKO MAEDA ◽  
HIROSHI FUJISAWA ◽  
CHARLES R. YURKON ◽  
YOSHIHIRO FUJII ◽  
...  
Keyword(s):  
Dna Repair ◽  
Cell Lines ◽  
Carbon Ions ◽  
Deficient Cell

scholarly journals a/alpha-control of DNA repair in the yeast Saccharomyces cerevisiae: genetic and physiological aspects.

Genetics ◽  
1993 ◽  
Vol 133 (3) ◽  
pp. 489-498 ◽  
Author(s):  
M Heude ◽  
F Fabre
Keyword(s):  
Dna Repair ◽  
Gamma Rays ◽  
Repair Process ◽  
Yeast Saccharomyces Cerevisiae ◽  
Dna Structures ◽  
Induced Mutagenesis ◽  
Error Prone Repair ◽  
G2 Phase ◽  
Mat Locus ◽  
Mat Genes

Abstract It has long been known that diploid strains of yeast are more resistant to gamma-rays than haploid cells, and that this is in part due to heterozygosity at the mating type (MAT) locus. It is shown here that the genetic control exerted by the MAT genes on DNA repair involves the a1 and alpha 2 genes, in a RME1-independent way. In rad18 diploids, affected in the error-prone repair, the a/alpha effects are of a very large amplitude, after both UV and gamma-rays, and also depends on a1 and alpha 2. The coexpression of a and alpha in rad18 haploids suppresses the sensitivity of a subpopulation corresponding to the G2 phase cells. Related to this, the coexpression of a and alpha in RAD+ haploids depresses UV-induced mutagenesis in G2 cells. For srs2 null diploids, also affected in the error-prone repair pathway, we show that their G1 UV sensitivity, likely due to lethal recombination events, is partly suppressed by MAT homozygosity. Taken together, these results led to the proposal that a1-alpha 2 promotes a channeling of some DNA structures from the mutagenic into the recombinational repair process.

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