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An SOS-inducible defective retronphage (phi R86) in Escherichia coli strain B.

作者信息

Kirchner J, Lim D, Witkin E M, Garvey N, Roegner-Maniscalco V

机构信息

Waksman Institute, Rutgers, State University of New Jersey, Piscataway 08553.

出版信息

Mol Microbiol. 1992 Oct;6(19):2815-24. doi: 10.1111/j.1365-2958.1992.tb01461.x.

Abstract

In Escherichia coli, RecA protein regulates the DNA damage-inducible survival-enhancing SOS response. Mutant allele recA730, which causes constitutive SOS expression, is lethal at high temperatures in B/r, a derivative of wild-type B, but not in K-12 or in certain B/r--K-12 hybrids. We present evidence that killing is due to SOS induction of a defective retronphage, phi R86, which is integrated into the B/r chromosome at 19 min, but is absent in K-12. phi R86 contains retron EC-86 which encodes reverse transcriptase and a small multicopy DNA-RNA complex, msDNA-RNA. Induction of phi R86 in recA730 B/r strains results in inhibition of host DNA replication before cell death. A retronphage 'killer' gene, ORF336, when overexpressed from a plasmid, causes similar effects without SOS induction. phi R86 is not detectably u.v.-inducible in recA+ strains.

摘要

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