AN SOS-INDUCIBLE DEFECTIVE RETRONPHAGE (PHI-R86) IN ESCHERICHIA-COLI STRAIN-B

被引:8
作者
KIRCHNER, J
LIM, DB
WITKIN, EM
GARVEY, N
ROEGNERMANISCALCO, V
机构
[1] STATE UNIV NEW JERSEY,WAKSMAN INST,PISCATAWAY,NJ 08553
[2] NYU MED CTR,DEPT MICROBIOL,NEW YORK,NY 10016
关键词
D O I
10.1111/j.1365-2958.1992.tb01461.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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, phiR86, which is integrated into the B/r chromosome at 19 min, but is absent in K-12. PhiR86 contains retron EC-86 which encodes reverse transcriptase and a small multicopy DNA-RNA complex, msDNA-RNA. Induction of phiR86 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. PhiR86 is not detectably u.v.-inducible in recA+ strains.
引用
收藏
页码:2815 / 2824
页数:10
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