Guanine and adenine analogues as tools in the investigation of the mechanisms of mismatch repair in E. coli.

摘要

The efficiency of in vivo correction of five "mismatch analogues", incorporated into M13mp9 DNA, was studied in an attempt to elucidate the structural determinants required for mismatch recognition by the repair machinery of E. coli. Inosine was efficiently removed from an I/T mismatch, presumably by the action of hypoxanthine glycosylase. The mismatch analogues DI/T (DI = 7-deazainosine), Tu/C (Tu = tubercidin), N/C (N = nebularine) and DN/C (DN = 7-deazanebularine) were left largely unrepaired, giving rise to high yields of mutant phenotype. The efficiency of correction of these mismatch analogues could be correlated with their structure within the base-pair.