Radicella J P, Clark E A, Chen S, Fox M S
Department of Biology, Massachusetts Institute of Technology, Cambridge 02139.
J Bacteriol. 1993 Dec;175(23):7732-6. doi: 10.1128/jb.175.23.7732-7736.1993.
In vivo experiments with heteroduplex lambda genomes show that the MutY mismatch repair system of Escherichia coli defines an average repair tract that is shorter than 27 nucleotides and longer than 9 nucleotides and extends 3' from the corrected adenine. The phenotype of a mutant defective in DNA polymerase I shows that this enzyme plays a significant, though not an essential, role in the in vivo repair of apurinic sites generated by this system. Evidence is presented that in the absence of polymerase I the repair tracts are modestly longer than in the polA+ extending in the 5' direction from the corrected adenine, suggesting a role for another DNA polymerase.