Genetic analysis of constitutive stable DNA replication in rnh mutants of Escherichia coli K12 |
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Authors: | Ted Albert Torrey and Tokio Kogoma |
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Institution: | (1) Department of Biology, University of New Mexico, 87131 Albuquerque, NM, USA;(2) Department of Cell Biology/Cancer Center, University of New Mexico, 87131 Albuquerque, NM, USA;(3) Present address: Roswell Park Memorial Institute, 666 Elm Street, 14263 Buffalo, NY, USA |
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Abstract: | Summary
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. |
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Keywords: | Stable DNA replication rnh rin recA lexA |
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