Hisao Masai and Ken-ichi Arai.

Department of Molecular and Developmental Biology, Institute of Medical Science, University of Tokyo, 4-6-1, Shirokanedai, Minato-ku, Tokyo, 108, Japan

Received 01/17/96; Accepted 02/17/96; On-line 03/01/96

The E. coli chromosome can be replicated in a manner independent of DnaA and oriC under certain conditions (Table 2). These altered modes of the chromosomal replication are called stable DNA replication (SDR), since they can continue stably in the absence of protein synthesis (27, 28). In the presence of DNA damaging agents or any treatment which temporarily halts the progression of replication forks, inducible SDR (iSDR) is observed. iSDR depends on RecA as well as on RecB and RecC. It is proposed that iSDR is initiated from a double-strand break (DSB) which is introduced in or near oriM (origin of SDR) (28). The linear end is converted to single-strand by exonuclease activity of RecBCD complex, which is assimilated into a D-loop by action of RecA protein (29). On the other hand, in an E. coli mutant which contains reduced activity of RNaseH encoded by rnhA, constitutive SDR (cSDR) is observed (30). cSDR is proposed to be initiated from R-loops, which are efficiently removed by rnhA-encoded RNaseH activity in the wild-type strain but persist in rnhA mutants. E. coli cells can survive lack of DnaA and/or oriC, when rnhA is mutated, indicating that growth of E. coli can be supported solely by cSDR. Then, what is the nature of the protein complex responsible for replication initiated from D-loops or R-loops?