An Immunoassay for Measuring Repair of UV Photoproducts

2014 ◽  
pp. 551-564 ◽  
Author(s):  
Shirley McCready
Keyword(s):  
Uv Photoproducts

UV Stimulation of Chromosomal Marker Exchange in Sulfolobus acidocaldarius: Implications for DNA Repair, Conjugation and Homologous Recombination at Extremely High Temperatures

Genetics ◽  
1999 ◽  
Vol 152 (4) ◽  
pp. 1407-1415 ◽  
Author(s):  
Katherine J Schmidt ◽  
Kristen E Beck ◽  
Dennis W Grogan
Keyword(s):  
Homologous Recombination ◽  
Incubation Temperature ◽  
Uv Light ◽  
Dna Lesions ◽  
Sulfolobus Acidocaldarius ◽  
Chromosomal Marker ◽  
Marker Exchange ◽  
Chromosomal Markers ◽  
Rate Of Decay ◽  
Uv Photoproducts

Abstract The hyperthermophilic archaeon Sulfolobus acidocaldarius exchanges and recombines chromosomal markers by a conjugational mechanism, and the overall yield of recombinants is greatly increased by previous exposure to UV light. This stimulation was studied in an effort to clarify its mechanism and that of marker exchange itself. A variety of experiments failed to identify a significant effect of UV irradiation on the frequency of cell pairing, indicating that subsequent steps are primarily affected, i.e., transfer of DNA between cells or homologous recombination. The UV-induced stimulation decayed rather quickly in parental cells during preincubation at 75°, and the rate of decay depended on the incubation temperature. Preincubation at 75° decreased the yield of recombinants neither from unirradiated parental cells nor from parental suspensions subsequently irradiated. We interpret these results as evidence that marker exchange is stimulated by recombinogenic DNA lesions formed as intermediates in the process of repairing UV photoproducts in the S. acidocaldarius chromosome.

A Dot Blot Immunoassay for UV Photoproducts

1999 ◽  
pp. 147-156
Author(s):  
Shirley McCready
Keyword(s):  
Dot Blot ◽  
Uv Photoproducts

scholarly journals Novel reagents for chemical cleavage at abasic sites and UV photoproducts in DNA

1995 ◽  
Vol 23 (10) ◽  
pp. 1664-1670 ◽  
Author(s):  
P. J. McHugh ◽  
J. Knowland
Keyword(s):  
Chemical Cleavage ◽  
Abasic Sites ◽  
Uv Photoproducts

Strand-Specific Modulation of UV Photoproducts in 5S rDNA by TFIIIA Binding and Their Effect on TFIIIA Complex Formation†

Biochemistry ◽  
1997 ◽  
Vol 36 (44) ◽  
pp. 13710-13717 ◽  
Author(s):  
Xiaoqi Liu ◽  
Antonio Conconi ◽  
Michael J. Smerdon
Keyword(s):  
Complex Formation ◽  
5S Rdna ◽  
Uv Photoproducts

scholarly journals Nucleotide Excision Repair in Human Cells

2013 ◽  
Vol 288 (29) ◽  
pp. 20918-20926 ◽  
Author(s):  
Jinchuan Hu ◽  
Jun-Hyuk Choi ◽  
Shobhan Gaddameedhi ◽  
Michael G. Kemp ◽  
Joyce T. Reardon ◽  
...  
Keyword(s):  
Nucleotide Excision Repair ◽  
Genomic Dna ◽  
Excision Repair ◽  
Human Cells ◽  
Naked Dna ◽  
Nucleotide Excision ◽  
Uv Photoproducts ◽  
Mutant Cells

Nucleotide excision repair is the sole mechanism for removing the major UV photoproducts from genomic DNA in human cells. In vitro with human cell-free extract or purified excision repair factors, the damage is removed from naked DNA or nucleosomes in the form of 24- to 32-nucleotide-long oligomers (nominal 30-mer) by dual incisions. Whether the DNA damage is removed from chromatin in vivo in a similar manner and what the fate of the excised oligomer was has not been known previously. Here, we demonstrate that dual incisions occur in vivo identical to the in vitro reaction. Further, we show that transcription-coupled repair, which operates in the absence of the XPC protein, also generates the nominal 30-mer in UV-irradiated XP-C mutant cells. Finally, we report that the excised 30-mer is released from the chromatin in complex with the repair factors TFIIH and XPG. Taken together, our results show the congruence of in vivo and in vitro data on nucleotide excision repair in humans.

DNA repair of UV photoproducts and mutagenesis in human mitochondrial DNA

1997 ◽  
Vol 273 (2) ◽  
pp. 417-427 ◽  
Author(s):  
B. Pascucci ◽  
A. Versteegh ◽  
A. van Hoffen ◽  
A.A. van Zeeland ◽  
L.H.F. Mullenders ◽  
...  
Keyword(s):  
Dna Repair ◽  
Mitochondrial Dna ◽  
Human Mitochondrial Dna ◽  
Uv Photoproducts

Mutagenesis induced by single UV photoproducts in E. coli and yeast

1993 ◽  
Vol 299 (3-4) ◽  
pp. 157-163 ◽  
Author(s):  
Christopher W. Lawrence ◽  
Peter E.M. Gibbs ◽  
Angela Borden ◽  
Michael J. Horsfall ◽  
Brian J. Kilbey
Keyword(s):  
E Coli ◽  
Uv Photoproducts

scholarly journals REV1 restrains DNA polymerase ζ to ensure frame fidelity during translesion synthesis of UV photoproducts in vivo

2008 ◽  
Vol 36 (21) ◽  
pp. 6767-6780 ◽  
Author(s):  
Dávid Szüts ◽  
Adam P. Marcus ◽  
Masayuki Himoto ◽  
Shigenori Iwai ◽  
Julian E. Sale
Keyword(s):  
Dna Polymerase ◽  
Translesion Synthesis ◽  
Uv Photoproducts

scholarly journals 1173 Inducible DNA repair of UV photoproducts depends on vitamin D receptor

2018 ◽  
Vol 138 (5) ◽  
pp. S199
Author(s):  
A. Scandurra ◽  
C. Wong ◽  
T. Kaur Oberoi ◽  
D. Oh
Keyword(s):  
Vitamin D ◽  
Dna Repair ◽  
Vitamin D Receptor ◽  
Uv Photoproducts

scholarly journals Binding of transcription factors creates hot spots for UV photoproducts in vivo

1992 ◽  
Vol 12 (4) ◽  
pp. 1798-1804
Author(s):  
G P Pfeifer ◽  
R Drouin ◽  
A D Riggs ◽  
G P Holmquist
Keyword(s):  
Transcription Factors ◽  
Hot Spots ◽  
Mammalian Cells ◽  
Phosphoglycerate Kinase ◽  
Promoter Sequence ◽  
Mean Value ◽  
Naked Dna ◽  
Dna Photoproducts ◽  
Uv Photoproducts

Cyclobutane dipyrimidines and less than mean value of 6-4 dipyrimidines are the two major classes of mutagenic DNA photoproducts produced by UV irradiation of cells. We developed a method to map cyclobutane dipyrimidines at the DNA sequence level in mammalian cells. The frequency of this class of photoproducts was determined at every dipyrimidine along the human phosphoglycerate kinase-1 (PGK1) promoter sequence and was compared to the UV-induced frequency distribution of mean value of 6-4 dipyrimidines. After irradiation of living cells containing active or inactive PGK1 genes, enzymatic or chemical cleavage at UV photoproducts, and amplification by ligation-mediated polymerase chain reaction, photofootprints were seen in all regions which bind transcription factors and appear as DNase I footprints. Photoproduct frequency within transcription factor binding sites was suppressed or enhanced relative to inactive genes or naked DNA with enhancements of up to 30-fold. Since photoproducts are mutagenic, this indicates that photoproduct (mutation?) hot spots may be tissue specific in mammals.

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