Multiple pathways for SOS-induced mutagenesis in Escherichia coli: An overexpression of dinB/dinP results in strongly enhancing mutagenesis in the absence of any exogenous treatment to damage DNA
- Su-Ryang Kim*,
- Geneviéve Maenhaut-Michel†,
- Masami Yamada*,
- Yoshihiro Yamamoto‡,
- Keiko Matsui*,
- Toshio Sofuni*,
- Takehiko Nohmi*, and
- Haruo Ohmori§,¶
- *Division of Genetics and Mutagenesis, National Institute of Health Sciences, Setagaya-ku, Tokyo 158, Japan; †Laboratoire de Génétique, Université Libre de Bruxelles, B1640 Rhode-St-Genèse, Belgium; ‡Department of Genetics, Hyogo College of Medicine, Nishinomiya, Hyogo 663, Japan; and §Institute for Virus Research, Kyoto University, Kyoto 606-01, Japan
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Edited by John R. Roth, University of Utah, Salt Lake City, UT, and approved October 6, 1997 (received for review February 18, 1997)
Abstract
dinP is an Escherichia coli gene recently identified at 5.5 min of the genetic map, whose product shows a similarity in amino acid sequence to the E. coli UmuC protein involved in DNA damage-induced mutagenesis. In this paper we show that the gene is identical to dinB, an SOS gene previously localized near the lac locus at 8 min, the function of which was shown to be required for mutagenesis of nonirradiated λ phage infecting UV-preirradiated bacterial cells (termed λUTM for λ untargeted mutagenesis). A newly constructed dinP null mutant exhibited the same defect for λUTM as observed previously with a dinB::Mu mutant, and the defect was complemented by plasmids carrying dinP as the only intact bacterial gene. Furthermore, merely increasing the dinP gene expression, without UV irradiation or any other DNA-damaging treatment, resulted in a strong enhancement of mutagenesis in F′lac plasmids; at most, 800-fold increase in the G6-to-G5 change. The enhanced mutagenesis did not depend on recA, uvrA, or umuDC. Thus, our results establish that E. coli has at least two distinct pathways for SOS-induced mutagenesis: one dependent on umuDC and the other on dinB/P.
Footnotes
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↵ ¶ To whom reprint requests should be addressed at: Institute for Virus Research, Kyoto University, Sakyo-ku, Kyoto 606–01, Japan. e-mail: hohmori{at}virus.kyoto-u.ac.jp.
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This paper was submitted directly (Track II) to the Proceedings Office.
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Abbreviations: UTM, untargeted mutagenesis; Lac+, lactose-fermenting.
- Copyright © 1997, The National Academy of Sciences of the USA





