Abstract
A number of mutants of E. coli defective in the ung gene (structural gene for uracil-deoxyribonucleic acid [ura-DNA] glycosylase) are shown to be abnormally sensitive to treatment with sodium bisulfite when compared with congenic ung+ strains. These results provide further evidence that sodium bisulfite causes the deamination of cytosine to uracil in DNA and that ura-DNA glycosylase is required for the repair of U-G mispairs. The effect of the chemical is apparently selective with respect to base damage; coliphages containing cytosine in their DNA are inactivated by treatment with sodium bisulfite, whereas those containing hydroxymethylcytosine are not. ura-DNA glycosylate and the major apurinic-apyrimidinic endonuclease of E. coli may function in the same repair pathway, since the extent of inactivation of a congenic set of strains which are ung xth (structural gene for the major apurinic-apyrimidinic endonuclease of E.coli) or ung xth+ is the same.
Original language | English (US) |
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Pages (from-to) | 1243-1252 |
Number of pages | 10 |
Journal | Journal of bacteriology |
Volume | 137 |
Issue number | 3 |
State | Published - Dec 1 1979 |
ASJC Scopus subject areas
- Microbiology
- Molecular Biology