## 1 Introduction  
A lambda (\(\lambda\)) prophage is maintained within the chromosome of _Escherichia coli_ (_E. coli_) by an action of the CI repressor encoded by gene _cl_. The inhibition of replication initiation from the prophage _ori_\(\lambda\) site positioned midway within gene \(O\)[1; 2; 3] (Figure 1A) is blocked by CI protein binding to operator sites overlapping promoters directing transcription leftward from _p_L, e.g., copying genes _N-int_, or rightward from _p_R for expressing genes _cro-clI-O-P-Q_. The product of gene \(P\) (gpP, P) participates in loading the _E. coli_ DnaB helicase [4] onto DNA during formation of a DnaB:P:O._ori_\(\lambda\) preprimosomal complex [5; 6; 7], each factor being required for replication initiation from _ori_\(\lambda\). DnaB unwinds double-stranded (ds) DNA at the replication fork, by encircling and translocating along the 5\({}^{\prime}\) lagging strand using energy provided by ATP hydrolysis [4]. The interaction between DnaGprimase and the N-terminal end of DnaB [8] increases both the NTPase and helicase activities of DnaB and the synthesis of RNA primers by DnaG [4; 8; 9; 10; 11; 12; 13; 14; 15]. DnaB can promote the progression of Holliday junctions, believed important in the repair of DNA damage occurring near advancing replication forks [16; 17]. DnaB functions as a hexamer, with about 20 hexamers per cell [18; 19], with each binding up to six ATP [20; 21]. It forms a complex with the host replication initiation protein DnaC to which the majority of DnaB in a cell is bound [22]. This interferes with the intrinsic single-stranded (ss) DNA binding activity of DnaB [20; 22; 23; 24; 25; 26]. The DnaC-DnaB complex acquires cryptic ssDNA binding activity specific to the bacterial origin of replication, _oriC_, where it begins unwinding dsDNA after a number of complex changes [27; 28; 29; 30; 31; 32; 33; 34]. The \(\lambda\) P protein has evolved to compete for and dissociate DnaC-DnaB complexes [5; 38] and two to six P monomers can bind to every DnaB hexamer [5; 39; 40], forming an enzymatically inactive \"dead-end\" complex [22]. High levels of P were found deleterious to host cells [41; 42] and it was  
Figure 1: Modes for expression of \(P\): (**A**) cryptic prophage map (for more \(\lambda\) gene detail refer to Figure 1B in reference [35] or Figure 1 in reference [36]); (**B**) \(\lambda\) gene expression is induced by shifting cells from 30 \({}^{\circ}\)C to 42 \({}^{\circ}\)C, which inactivates the encoded Ts (temperature sensitive) _c1_[Ts]857 repressor, permitting rightward transcription from promoter \(p\)R; and (**C**) an exact copy of \(P\) (or alleles of \(P\)) was cloned into the synthetic expression plasmid pclpR-timm [35] (shown by arrows at ATG and TAA). \(P\) expression from pclpR-\(P\)-imm is controlled by the \(\lambda\) CI[Ts] repressor. The circle to the right of \(p\)R and left of ATG represents the ribosomal binding site for the deleted intervening gene _cro_. The transcription of \(P\) from the plasmid terminates at the transcriptional terminator _timm_, which in the wild type \(\lambda\) sequence prevents both the low maintenance and high level establishment modes of _cl-rexA-rexB_ transcription from transcribing leftward from \(p\)M or \(p\)E into _oL-pL_[37]. suggested that P sequestered, _i.e._, bound-up, DnaB and thus interfered with the initiation of host DNA synthesis. ColE1 replication establishment or propagation [43] is extremely sensitive to P [35]. The effect is suppressed by alleles of _dnaB_ or \(P\), which suggests that P can impact a cellular replication event by acting outside of the DnaA and _oriC_-dependent replication initiation step. This same study showed that P-dependent cellular filamentation arose in cells defective for SOS induction, suggesting that P was influencing replication propagation or restart mechanisms.