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CYCLOBUTANE DIMERS AND (6‐4)PHOTOPRODUCTS IN HUMAN CELLS ARE MENDED WITH THE SAME PATCH SIZES
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AbstractThe sizes of excision repair patches corresponding to excision of (6‐4) pyrimidine‐pyrimidone photoproducts and (5‐5,6–6) cyclobutane dimers have been independently determined by using bromodeoxyuridine substitution and density increases in isopycnic gradients of small DNA fragments. The two classes of photoproducts were distinguished by using (a) a xeroderma pigmentosum (XP) revertant cell line that excises (6‐4) photoproducts normally, but does not excise cyclobutane dimers from bulk DNA or from an actively transcribed sequence; (b) an XP cell line containing the denV gene of bacteriophage T4, which repairs only cyclobutane dimers by a unique glycosylase mechanism, and (c) normal cells analyzed during time intervals in which cyclobutane dimer repair is the main repair process in action. The patch sizes for the two lesions were similar under all conditions and were estimated to be approximately30–40 bases. These values are slightly larger than corresponding estimates for Escherichia coli and Saccharomyces cerevisiae but close to estimates from in vitro experiments with human cell extracts. The size of 30 bases may consequently be very close to the actual distance between cleavage sites made on either side of a photoproduct during repair.
Title: CYCLOBUTANE DIMERS AND (6‐4)PHOTOPRODUCTS IN HUMAN CELLS ARE MENDED WITH THE SAME PATCH SIZES
Description:
AbstractThe sizes of excision repair patches corresponding to excision of (6‐4) pyrimidine‐pyrimidone photoproducts and (5‐5,6–6) cyclobutane dimers have been independently determined by using bromodeoxyuridine substitution and density increases in isopycnic gradients of small DNA fragments.
The two classes of photoproducts were distinguished by using (a) a xeroderma pigmentosum (XP) revertant cell line that excises (6‐4) photoproducts normally, but does not excise cyclobutane dimers from bulk DNA or from an actively transcribed sequence; (b) an XP cell line containing the denV gene of bacteriophage T4, which repairs only cyclobutane dimers by a unique glycosylase mechanism, and (c) normal cells analyzed during time intervals in which cyclobutane dimer repair is the main repair process in action.
The patch sizes for the two lesions were similar under all conditions and were estimated to be approximately30–40 bases.
These values are slightly larger than corresponding estimates for Escherichia coli and Saccharomyces cerevisiae but close to estimates from in vitro experiments with human cell extracts.
The size of 30 bases may consequently be very close to the actual distance between cleavage sites made on either side of a photoproduct during repair.
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