Ossanna N, Mount D W
Department of Molecular and Cellular Biology, University of Arizona, Tucson 85721.
J Bacteriol. 1989 Jan;171(1):303-7. doi: 10.1128/jb.171.1.303-307.1989.
We have isolated three new mutations in uvrD that increase expression of the Escherichia coli SOS response in the absence of DNA damage. Like other uvrD (DNA helicase II) mutants, these strains are sensitive to UV irradiation and have high spontaneous mutation frequencies. Complementation studies with uvrD+ showed that UV sensitivity and spontaneous mutator activity were recessive in these new mutants. The SOS-induction phenotype, however, was not completely complemented, which indicated that the mutant proteins were functioning in some capacity. The viability of one of the mutants in combination with rep-5 suggests that the protein is functional in DNA replication. We suggest that these mutant proteins are deficient in DNA repair activities (since UV sensitivity is complemented) but are able to participate in DNA replication. We believe that defective DNA replication in these mutants increases SOS expression.
我们分离出了uvrD中的三个新突变,这些突变在没有DNA损伤的情况下会增加大肠杆菌SOS反应的表达。与其他uvrD(DNA解旋酶II)突变体一样,这些菌株对紫外线照射敏感,且自发突变频率很高。用uvrD+进行的互补研究表明,紫外线敏感性和自发诱变活性在这些新突变体中是隐性的。然而,SOS诱导表型并未完全互补,这表明突变蛋白在某种程度上仍在发挥作用。其中一个突变体与rep-5组合后的生存能力表明该蛋白在DNA复制中具有功能。我们认为这些突变蛋白在DNA修复活性方面存在缺陷(因为紫外线敏感性得到了互补),但能够参与DNA复制。我们相信这些突变体中存在缺陷的DNA复制会增加SOS的表达。