Abstract
Cytosine spontaneously deaminates to form uracil, generating G/U pairs in DNA. We studied the repair of these lesions by introducing specific G/U pairs into the genome of SV40 and determining the fate of the mispaired bases in Simian cells. Analysis of 135 plaques obtained after transfection of the modified viral DNA indicates that G/U lesions were repaired to G/C in every case. This result indicates that G/U lesions are corrected with greater efficiency and specificity than any combination of DNA base/base mispairs, in transfected SV40 DNA.
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