## 2 Result and Discussions
### 1. P-Dependent Cellular Filamentation  
We previously observed extensive cellular filamentation upon the de-repression of \(\lambda cI\)[Ts]857\(O\)am8 prophage, but not for a \(\lambda cI\)[Ts]857\(P\)am3 prophage in lysogenic cells [31]. [PERSON] and [PERSON] [23] demonstrated that expression of \(P\) from a plasmid can cause cellular filamentation, which they attributed to an ability of P to impair bacterial DNA synthesis. Agents that block cellular DNA synthesis can stimulate a cellular SOS response [86], which in turn elevates expression of one of the SOS response genes, _suLA_, whose product prevents the action of FtsZ at the site of septum formation, causing a cell to stop dividing [89, 90], and allows time for DNA repair (see [91]). Cells inhibited for  
\begin{table}
\begin{tabular}{l c c c c c c c c c c c c} \hline
**Strain [plasmid]** & \multicolumn{2}{c}{**Time**} & \multicolumn{8}{c}{**Relative cell length**} & \multicolumn{2}{c}{**Sum**} \\  & & **(Temp)** & & & & & & & & & & **cells** \\  & & & **1X** & **2X** & **3X** & **4X** & **5X** & **6X** & **7X** & **8X** & **9X** & \(\geq\)**10X** & \\ \hline
594 & & 0 (25) & 26 & 19 & 0 & 0 & 0 & 0 & 0 & 0 & 0 & 0 & 45 \\  & \({}^{\rm{cc}}\) & & 1 (42) & 15 & 11 & 11 & 8 & 0 & 0 & 0 & 0 & 0 & 0 & 45 \\  & \({}^{\rm{cc}}\) & & 3 (42) & 28 & 15 & 2 & 0 & 0 & 0 & 0 & 0 & 0 & 0 & 45 \\  & \({}^{\rm{cc}}\) & & 5 (42) & 29 & 14 & 2 & 0 & 0 & 0 & 0 & 0 & 0 & 0 & 45 \\ \hline
594 _lexA3_ & & 0 (25) & 40 & 32 & 2 & 0 & 0 & 0 & 0 & 0 & 0 & 0 & 74 \\  & \({}^{\rm{cc}}\) & & 1 (42) & 23 & 16 & 6 & 0 & 0 & 0 & 0 & 0 & 0 & 0 & 45 \\  & \({}^{\rm{cc}}\) & & 3 (42) & 31 & 13 & 1 & 0 & 0 & 0 & 0 & 0 & 0 & 0 & 45 \\  & \({}^{\rm{cc}}\) & & 5 (42) & 42 & 3 & 0 & 0 & 0 & 0 & 0 & 0 & 0 & 0 & 45 \\ \hline
594 _lexA3_[pclpR-\(P\)-timm] & 0 (25) & 71 & 19 & 0 & 0 & 0 & 0 & 0 & 0 & 0 & 0 & 90 \\  & \({}^{\rm{cc}}\) & & 1 (37) & 21 & 23 & 1 & 0 & 0 & 0 & 0 & 0 & 0 & 0 & 45 \\  & \({}^{\rm{cc}}\) & & 3 (37) & 7 & 9 & 9 & 6 & 4 & 3 & 2 & 1 & 2 & 2 & 45 \\  & \({}^{\rm{cc}}\) & & 5 (37) & 6 & 20 & 0 & 0 & 2 & 0 & 3 & 3 & 3 & 8 & 45 \\ \hline
594 _lexA3_[pclpR-\(P\)-timm] & 1 (42) & 9 & 19 & 13 & 3 & 1 & 0 & 0 & 0 & 0 & 0 & 0 & 45 \\  & \({}^{\rm{cc}}\) & & 3 (42) & 11 & 1 & 3 & 4 & 4 & 9 & 8 & 2 & 2 & 1 & 45 \\  & \({}^{\rm{cc}}\) & & 5 (42) & 8 & 6 & 7 & 1 & 1 & 0 & 2 & 1 & 2 & 14 & 42 \\ \hline
594 [pHB30] & 0 (30) & 6 & 20 & 4 & 0 & 0 & 0 & 0 & 0 & 0 & 0 & 0 & 30 \\  & \({}^{\rm{cc}}\) & & 1 (42) & 0 & 2 & 10 & 9 & 3 & 4 & 1 & 1 & 0 & 0 & 30 \\  & \({}^{\rm{cc}}\) & & 3 (42) & 2 & 4 & 8 & 3 & 2 & 5 & 2 & 1 & 2 & 1 & 30 \\  & \({}^{\rm{cc}}\) & & 5 (42) & 2 & 8 & 10 & 2 & 2 & 2 & 3 & 0 & 0 & 1 & 30 \\ \hline
594 _lexA_ [pHB30] & 0 (30) & 5 & 17 & 8 & 0 & 0 & 0 & 0 & 0 & 0 & 0 & 30 \\  & \({}^{\rm{cc}}\) & & 1 (42) & 0 & 6 & 6 & 8 & 4 & 1 & 4 & 0 & 1 & 0 & 30 \\  & \({}^{\rm{cc}}\) & & 3 (42) & 3 & 5 & 2 & 6 & 4 & 0 & 5 & 3 & 1 & 1 & 30 FtsZ activity form filaments that are longer than dividing cells. Induction defective mutations in _lexA_ encoding the repressor for the SOS response, or certain _recA_ mutations prevent the induction of a cellular SOS response [86]. The hypothesis that P-lethality does not involve an interaction between P and DnaB, but is instead targeted to DnaA, implies that the P:DnaA interaction can prevent _E. coli_ replication initiation at _oriC_ by removing available DnaA. Previous studies have shown that a _dnaA_46[Ts] mutant exhibits a slow-stop effect on DNA synthesis when the cells are shifted to 42 \({}^{\circ}\)C, blocking re-initiation at _oriC_; however, these cells continue to divide, forming anucleate cells, not filaments [92,93]. Other cellular interactions beyond those between DnaA or DnaB and P are important. For example, as noted, P interacts with DnaK and DnaJ. The inactivation of _dnaK_, and apparently _dnaJ_, results in multiple cellular defects, including formation of cell filaments, abnormally segregated chromosomes, and loss of plasmid maintenance [94]. Does P function in replication restart?