Torrey T A, Kogoma T
Department of Biology, University of New Mexico, Albuquerque 87131.
Mol Gen Genet. 1987 Jul;208(3):420-7. doi: 10.1007/BF00328133.
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.
缺乏核糖核酸酶H（RNase H）的大肠杆菌rnh突变体能够在无蛋白质合成的情况下进行DNA复制。这种组成型稳定DNA复制（SDR）依赖于recA +基因产物。SDR对recA +的需求可被rin突变（用于不依赖recA +）或使LexA阻遏物失活的lexA（Def）突变所抑制。因此，rnh突变体中至少存在三种遗传上不同类型的SDR：在rnh - rin + lexA +菌株中可见的recA +依赖性SDR，在rnh - rin - lexA +中不依赖recA +，以及在rnh - rin + lexA（Def）中不依赖recA +。rin和lexA（Def）突变体中SDR的表达表明需要RNA合成且不存在RNase H。已表明rin突变对recA +需求的抑制取决于recF +基因产物的某些新功能。相比之下，lexA -（Def）突变的抑制不依赖于recF +。lexA3突变通过减少可用的recA +活性量来抑制recA +依赖性SDR，并被recAo254突变所抑制。rnh - rin -细胞中的SDR也被lexA3突变所抑制，但recAo254突变不能逆转这种抑制，这表明在不依赖recA +的SDR过程中需要一些其他受lexA +调节的基因产物。本文提出了一个由lexA +、rin +和recF +基因产物调控这三种类型SDR表达的模型。
