Physical mapping and characterization of the mitochondrial DNA and RNA sequences from mit- mutants defective in cytochrome oxidase peptide 1 (OXI 3). |
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| Authors: | Richard Morimoto Alfred Lewin Murray Rabinowitz |
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| Affiliation: | (1) Department of Medicine, The University of Chicago, 60637 Chicago, Illinois, USA;(2) Department of Biology, The University of Chicago, 60637 Chicago, Illinois, USA;(3) Department of Biochemistry, The University of Chicago, 60637 Chicago, Illinois, USA;(4) The Franklin McLean Memorial Research Institute, The University of Chicago, 60037 Chicago, Illinois, USA;(5) Present address: The Biological Laboratories, Harvard University, 02138 Cambridge, MA;(6) Present address: Biozentrum, Universität Basel, Basel, Switzerland |
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| Abstract: | Summary The striking similarity between the treatments that induce SOS functions and those that result in stable DNA replication (continuous DNA replication in the absence of protein synthesis) prompted us to examine the possibility of stable DNA replication being a recA+lexA+-dependent SOS function. In addition to the treatments previously reported, ultraviolet (UV) irradiation or treatment with mitomycin C was also found to induce stable DNA replication.The thermal treatment of tif-1 strains did not result in detectable levels of stable DNA replication, but nalidixic acid readily induced the activity in these strains. The induction of stable DNA replication with nalidixic acid was severely suppressed in tif-1 lexA mutant strains. The inhibitory activity of lexA3 was negated by the presence of the spr-51 mutation, an intragenic suppressor of lexA3.Induced stable DNA replication was found to be considerably more resistant to UV irradiation than nromal replication both in a uvrA6 strain and a uvr+ strain. The UV-resistant replication occurred mostly in the semiconservative manner. The possible roles of stable DNA replication in repair of damaged DNA are discussed. |
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