An SOS‐inducible defective retronphage (φR86) in Escherichia coli strain B

Summary In Escherichia coli, RecA protein regulates the DNA damage‐inducible survival‐enhancing SOS response. Mutant aliele 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 presen...

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Veröffentlicht in:Molecular microbiology 1992-10, Vol.6 (19), p.2815-2824
Hauptverfasser: Kirchner, Jakob, Lim, Dongbin, Witkin, Evelyn M., Garvey, Nancy, Roegner‐Maniscalco, Vivien
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Sprache:eng
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Zusammenfassung:Summary In Escherichia coli, RecA protein regulates the DNA damage‐inducible survival‐enhancing SOS response. Mutant aliele 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, φR86, which is integrated into the B/r chromosome at 19 min, but is absent in K‐12. φR86 contains retron EC‐86 which encodes reverse transcriptase and a small multicopy DNA‐RNA complex, msDNA‐RNA. Induction of φR86 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. φR86 is not detectably u.v.‐inducible in recA* strains.
ISSN:0950-382X
1365-2958
DOI:10.1111/j.1365-2958.1992.tb01461.x