Tadmor Y, Ascarelli-Goell R, Skaliter R, Livneh Z
Department of Biochemistry, Weizmann Institute of Science, Rehovot, Israel.
J Bacteriol. 1992 Apr;174(8):2517-24. doi: 10.1128/jb.174.8.2517-2524.1992.
Overproduction of the beta 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 alpha 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 beta on UV mutagenesis. We have previously suggested that DNA polymerase III holoenzyme can exist in two forms: beta-rich form unable to bypass UV lesions and a beta-poor form capable of bypassing UV lesions (O. Shavitt and Z. Livneh, J. Biol. Chem. 264:11275-11281, 1989). The beta-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 beta subunit affects the relative abundance of the regular replicative beta-rich polymerase and the SOS bypass-proficient polymerase by sequestering the polymerase molecules to the beta-rich form and blocking the SOS form.
DNA聚合酶III全酶β亚基的过量表达导致紫外线诱变率降低5至10倍,同时大肠杆菌对紫外线的敏感性略有增加。在切除缺陷型细胞中也观察到了同样的效果,排除了这些影响是通过切除修复的变化介导的可能性。相比之下,聚合酶α亚基的过量表达既不影响紫外线诱变,也不影响紫外线敏感性。从质粒表达的诱变蛋白MucA和MucB的存在减轻了过量表达的β亚基对紫外线诱变的影响。我们之前曾提出,DNA聚合酶III全酶可以以两种形式存在:富含β亚基的形式无法绕过紫外线损伤,而β亚基含量低的形式能够绕过紫外线损伤(O. Shavitt和Z. Livneh,《生物化学杂志》264:11275-11281,1989)。β亚基含量低的形式可能与DNA聚合酶III的SOS形式有关,该形式旨在在SOS条件下进行跨损伤聚合,从而产生突变。基于此模型,我们提出过量表达的β亚基通过将聚合酶分子隔离到富含β亚基的形式并阻断SOS形式,影响常规复制性富含β亚基的聚合酶和SOS旁路 proficient聚合酶的相对丰度。