Genetic analysis of constitutive stable DNA replication in rnh mutants of Escherichia coli K12.
Escherichia coli rnh mutants deficient in ribonuclease H (RNase H) are capable of DNA replication in the absence of protein synthesis. This constitutive stable DNA replication (SDR) is dependent upon the recA+ gene product. The requirement of SDR for recA+ can be suppressed by rin mutations (for recA+-independent), or by lexA(Def) mutations which inactivate the LexA repressor. Thus, there are at least three genetically distinct types of SDR in rnh mutants: recA+-dependent SDR seen in rnh- rin+ lexA+ strains, recA+-independent in rnh- rin- lexA+, and recA+-independent in rnh- rin+ lexA(Def). The expression of SDR in rin- and lexA(Def) mutants demonstrated a requirement for RNA synthesis and for the absence of RNase H. The suppression of the recA+ requirement by rin mutations was shown to depend on some new function of the recF+ gene product. In contrast, the suppression by lexA-(Def) mutations was not dependent on recF+. The lexA3 mutation inhibited recA+-dependent SDR via reducing the amount of recA+ activity available, and was suppressed by the recAo254 mutation. The SDR in rnh- rin- cells was also inhibited by the lexA3 mutation, but the inhibition was not reversed by the recAo254 mutation, indicating a requirement for some other lexA+-regulated gene product in the recA+-independent SDR process. A model is presented for the regulation of the expression of these three types of SDR by the products of the lexA+, rin+ and recF+ genes.
Torrey
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TA
Department of Biology, University of New Mexico, Albuquerque 87131.
Kogoma
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D004261:DNA Replication; D004722:Endoribonucleases / Q000235:genetics*; D004926:Escherichia coli / Q000201:enzymology / Q000235:genetics* / Q000254:growth & development; D005838:Genotype; D007700:Kinetics; D009154:Mutation; D016914:Ribonuclease H; D013045:Species Specificity; D013696:Temperature
D004722:Endoribonucleases; D016914:Ribonuclease H