Co-Authors:
Tadmor, Y., Department of Biochemistry, Weizmann Institute of Science, Rehovot 76100, Israel
Ascarelli-Goell, R., Department of Biochemistry, Weizmann Institute of Science, Rehovot 76100, Israel
Skaliter, R., Department of Biochemistry, Weizmann Institute of Science, Rehovot 76100, Israel
Livneh, Z., Department of Biochemistry, Weizmann Institute of Science, Rehovot 76100, Israel
Abstract:
Overproduction of the β subunit of DNA polymerase III holoenzyme caused a 5- to 10-fold reduction of UV mutagenesis along with a slight increase in sensitivity to UV light in Escherichia coli. The same effects were observed in excision-deficient cells, excluding the possibility that they were mediated via changes in excision repair. In contrast, overproduction of the α subunit of the polymerase did not influence either UV mutagenesis or UV sensitivity. The presence of the mutagenesis proteins MucA and MucB expressed from a plasmid alleviated the effect of overproduced β on UV mutagenesis. We have previously suggested that DNA polymerase III holoenzyme can exist in two forms: β-rich form unable to bypass UV lesions and a β-poor form capable of bypassing UV lesions (O. Shavitt and Z. Livneh, J. Biol. Chem. 264:11275- 11281, 1989). The β-poor form may be related to an SOS form of DNA polymerase III designed to perform translesion polymerization under SOS conditions and thereby generate mutations. On the basis of this model, we propose that the overproduced β subunit affects the relative abundance of the regular replicative β-rich polymerase and the SOS bypass-proficient polymerase by sequestering the polymerase molecules to the β-rich form and blocking the SOS form.