## 1 Introduction
Shifting cells with a pclpR-[GOI]-timm plasmid that were grown at 25 or 30 \({}^{\circ}\)C, to above 39 \({}^{\circ}\)C induces expression of the GOI from the plasmid [20]. (**B**) Cryptic prophage in strain Y836. The \(\lambda\) phage genes _cro-cII-O-P-ren_ are transcribed from promoter _pR_ that is embedded within the rightward operator sequence, _oR_, between genes _cI_ and _cro_. Gene _cI_, encoding a temperature sensitive repressor is transcribed from promoter _pM_; and _cro_ is transcribed in the opposite direction from _pR_. C. At temperatures where CI remains active, i.e., at or below 38 \({}^{\circ}\)C, \(\lambda\) replication initiation is prevented, and the \(\lambda\) fragment is replicated as part of the _E. coli_ chromosome by forks arising from _oriC_. At about 39 \({}^{\circ}\)C, CI becomes fully denatured, _pR_ transcription is induced, and \(\lambda\) undergoes a few replication initiation events from _ori\(\lambda\)_[22]. [PERSON] and [PERSON] [23] examined the effect of cloning the \(\lambda\) fragment sequence bp's \(39168-44972\) (part of \(O\), _P-ren_-and downstream _orf's 290-146-57-56-60-204-68-64_) into a plasmid expression vector regulated by the _lac_ promoter. They showed that inducing \(P\) expression correlated with effects of shifting cells with temperature sensitive slow-stop mutations in replication initiation genes to the non-permissive temperature, i.e., an eventual inhibition in _E. coli_ replication was seen after about a 50 min induction. The effect paralleled the addition of chloramphenicol, and was opposite the effect of adding nalidixic acid, which produced an immediate (fast-stop) inhibition in chromosomal replication (their Figure 5). [PERSON] _et al._[24] cloned \(\lambda\) genes into pBR322 and followed the survival of bacteria after transformation with a plasmid that constitutively expressed _pR-cro-O-P-ren-tR2_, measuring transformants (Amp\({}^{\rm R}\) colony forming units, cfu) per \(\mu\)g DNA. They observed that plasmids expressing active \(P\) did not yield survivor cfu, concluding that \(P\) expression is lethal to the host, i.e., P-lethality. They found that three types of _groP_ mutants of _E.coli_, which do not allow \(\lambda\) DNA replication, possibly due to the lack of interaction of P protein with the altered DnaB (_gro_PA15, _gro_PB558) or DnaJ protein (_gro_PC259), were equally susceptible to killing by P protein. They concluded that P-lethality _does not involve interaction of_ P with the host DnaB, DnaJ, or DnaK proteins, which are all essential for \(\lambda\) DNA replication [25-27] but is targeted to the _E. coli_ DNA replication initiation protein DnaA, inhibiting its _oriC_ DNA binding [28]. [PERSON] _et al._[29] identified mutations within the gene _dnaA_ that confer cellular resistance to P-lethality. An alternative hypothesis for the absence of transformants formed by plasmids expressing \(P\) was not considered in prior studies, i.e., that \(P\) expression from the transformed pBR322-derived plasmids employed interfered with / blocked the initiation of plasmid replication and copy increase within the newly transformed cell. Since the replication origin of pBR322 was derived from pMB1, closely related to ColE1 [30] we refer herein to the plasmids employed as ColE1-type plasmids. In the present manuscript we examine if the interaction of P and DnaB provides an alternative mechanism for P-lethality. We assess the influence of P expression upon the maintenance of ColE1 plasmids, and we examine whether P expression, shown to stimulate cellular filamentation, depends upon triggering a cellular SOS response. Figure 1: _Cont._