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Nucleic Acids Research, 1985, Vol. 13, No. 1 303-315
© 1985

Articles

Recognition of a cytosine base lesion by a human damage-specific DNA binding protein

Josephine A. Carew1 and Ross S. Feldberg*

Department of Biology, Tufts University Medford, MA 02155, USA

*To whom all correspondence should be addressed

Received March 20, 1984. Revised September 29, 1984. Accepted November 19, 1984.

Sodium bisulfite reacts with cytosine and 5-methylcytosine, forming the 5,6-dihydrosulfonate adducts which deaminate to the uracil and thymine adducts, respectively. At alkaline pH, the sulfonate groups are then released, generating uracil and thymine. In DNA, the resulting G:U and G:T base mismatches generated are potential sites of mutagenesis. Using a human damage-specific DNA binding protein as a probe, we have found proteinrecognizable lesions in bisulfite-treated DNA and poly d(I–C), but not in treated poly d(A–T) or poly d(A–U). Although this suggests that the lesion recognized is cytosine-derived, there was no correlation between the number of uracils induced and the number of binding sites, suggesting that the proteinbound damage is not a uracil-containing mismatch. Modification of the treatment protocol to reduce elimination of the bisulfite from the base adducts increased the level of binding, suggesting that the protein recognizes a base-sulfonate adduct.

1Present address: Laboratory of Radiobiology, Harvard School of Public Health, Boston, MA 02155


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