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ALKALI‐LABILE PHOTOLESIONS MAPPING TO PURINE SITES IN ULTRAVIOLET‐IRRADIATED DNA
Author(s) -
Hejmadi Vidyasagar,
Stevenson Clarke,
Kumar Shiv,
Davies R. Jeremy H.
Publication year - 1994
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.1994.tb05022.x
Subject(s) - thymine , dna , oligonucleotide , chemistry , purine metabolism , cleavage (geology) , purine , pyrimidine , cytosine , nucleotide , stereochemistry , biochemistry , enzyme , biology , gene , paleontology , fracture (geology)
Gel sequencing experiments with the 5′‐ and 3′‐end‐labeled oligonucleotides d(A 3 GA 4 GA 5 GA 6 GA 3 G) and d(AT) 10 have demonstrated that dimeric adenine photoproducts and thymine‐adenine photoadducts constitute alkali‐labile lesions in UV‐irradiated DNA. On treatment with hot piperidine, DNA strand breakage occurs predominantly at the sites of 5′‐adenines in the dimeric photoproducts and of 3′‐adenines in the thymine‐adenine photoadducts. With 5′‐end‐labeled oligonucleotides of mixed sequence, major UV‐induced loci for alkaline cleavage map to purine bases flanked on their 5′‐side by two pyrimidines. This behavior does not arise from enhanced photoreactivity of purines in this sequence context as has been inferred from photofootprinting studies. Instead, as shown by 3′‐labeling and selective substitution with 5‐methylcytosine, it results from the anomalous electrophoretic mobility of 5′‐end‐labeled fragments produced by alkaline cleavage of DNA at adjacent pyrimidine (6‐4) pyrimidone photoproducts.