The C-C (6-4) UV photoproduct is mutagenic in Escherichia coli.

Glickman, Barry W.; Schaaper, Roel M.; Haseltine, William A.; Dunn, Ronnie L.; Brash, Douglas E.

doi:10.1073/pnas.83.18.6945

Cited by 90 publications

(53 citation statements)

References 36 publications

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“…5-Methylcytosines replace normal cytosines in CpG dinucleotides at the PGKJ promoter when the gene is on the inactive X chromosome (40) and inhibit <6-4> DP formation at these positions (37). We report, in accord with others (21), that 5-methylcytosines participate in formation of cyclobutane DPs about as much as do cytosines at the same sequence positions (Fig. 3B).…”

Section: Methodssupporting

confidence: 75%

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

Pfeifer¹,

Drouin²,

Riggs³

et al. 1992

Mol. Cell. Biol.

154

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Cyclobutane dipyrimidines and <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 (PGKI) promoter sequence and was compared to the UV-induced frequency distribution of <6-4> dipyrimidines. The formation of DNA photoproducts by UV light is implicated in induction of mutations and the development of skin cancer (1,10,16,24,32,33). Because of a lack of sufficiently sensitive techniques, the susceptibility of specific DNA sequences to form photoproducts has heretofore been analyzed almost exclusively with cloned DNA, and very little is known about the effects of DNA sequence and chromatin structure on photoproduct formation in mammalian cells. Becker and Wang introduced a NaBH4-aniline technique to break DNA at virtually all classes of UVinduced photoproducts (4, 5). These photoproduct classes are, in order of their relative frequency, (i) cyclobutane dipyrimidines (cyclobutane DPs), which involve two covalent bonds between adjacent pyrimidines; (ii) pyrimidine <6-4> pyrimidone photoproducts (<6-4> dipyrimidines [<6-4> DPs]), which involve a single covalent bond between positions 6 and 4 of adjacent pyrimidines; (iii) rare monoadducts, usually involving photoaddition of H-or HO-to the double bonds at positions 5 and 6 of pyrimidines (6); and (iv) rare TpA and ApA dimers (7,8,19,20,28). End-labeled DNA was size fractionated on sequencing gels to reveal the sequence position of these photoproducts. Selleck and Majors (42) used the Church and Gilbert (14) genomic sequencing technique on in vivo UV-irradiated yeast DNA to reveal the sequence positions of NaBH4-aniline labile photoproducts. Subsequently, they used end-labeled primers for multiple primer extensions with Taq polymerase (2).The polymerase stopped almost exclusively at dipyrimidine photoproducts yielding a sequence ladder reflecting photoproduct frequency of both cyclobutane DPs and <6-4> DPs along the UV-irradiated yeast genome. We recently used an exponential amplification method, the ligation-mediated polymerase chain reaction (LM-PCR) (35, 39), to map photoproducts which can be converted into ligatable DNA breaks (37). Pyrimidine <6-4> pyrimidone photoproducts were specifically cleaved with alkaline piperidine (29 The frequency with which a particular nucleotide or dinucleotide will be involved in a particular class of photoreaction may be affected by flanking sequence, methylation state of cytidines, and bound proteins. These factors are expected to combine to produce photoproduct hot spots and cold spots along the genome. In previous studies, we determined the sequence, cytidine methylation status, and DNase I footprints due to transcription factors or nucleosomes along the promoter of active and inactive PGKJ genes (38)(39)(40). Here, we have determined the influence of...

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Section: Methodssupporting

confidence: 75%

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

Pfeifer¹,

Drouin²,

Riggs³

et al. 1992

Mol. Cell. Biol.

154

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“…This is a much higher level than previously determined (Mitchell et al 1990a). Several studies indicate that the (6-4) photoproduct is more mutagenic than the cyclobutane dimer (Franklin & Haseltine 1986;Glickman et al 1986;Tang et al 1986;Brash 1988;Mitchell et al 1990a). Polycromatic UV light inhibits the mitotic activity and leads to superficial nuclear fragmentation of the rat corneal epithelium (Buschke et al 1945).…”

mentioning

confidence: 56%

UVB‐induced formation of (6–4) photoproducts in the rat corneal epithelium

Estil

Olsen

Huitfeldt

et al. 1997

Acta Ophthalmologica Scandinavica

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ABSTRACT. The induction of DNA photoproducts in rat corneal epithelium was studied after in vivo exposure to different doses of ultraviolet B light at 297 nm. Affinity-purified antibodies with a major specificity against UV-induced (6-4) photoproducts were used. The results indicate a dose dependent formation of (6-4) photoproducts. Even a minimal erythema dose (25 mJ/cm2) produced (6-4) photoproducts, demonstrating that DNA damage occurs in corneal tissue following exposure to biologically relevant doses of UVB light.

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“…Brash and Haseltine (13) have suggested that the predominance of G-C -* AT transitions among nonsense mutations in the lacd gene is due to the mutagenic potential of the (6-4) lesion. More recently, Glickman et al (14) have presented data indicating perhaps two-thirds or more of UV-induced mutation in E. coli is due to this photoproduct. Similar conclusions about the predominance of (6-4) photoproduct-induced transitions have been reached following the sequencing of several hundred lacd mutants in both Uvr' and UvrB-strains of E. coli (15).…”

Section: Discussionmentioning

confidence: 99%

“…However, the relative roles of the two major UV photoproducts, the (6-4) pyrimidine pyrimidone lesion and the cyclobutane dimer, remain controversial especially in mammalian cells. Evidence that the (6-4) lesion may play a dominant role in UV-induced transition mutagenesis has been obtained for bacteria (13)(14)(15) and X phage (16). However, there is evidence that cyclobutane dimers are also capable of targeting mutation in both bacteria (17) and mammalian cells (18).…”

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confidence: 99%