Table 4.

Suppression of CII toxicity and plasmid loss by oop expression in rpoB mutants.

Host Strains with rpoB Alleles	Cell Viability (±SE) [% Plasmid Loss] Per Growth of Transformant at 42 °C
	[cII] a	[cII-oop-pO94] b
594 c	<0.001 (0.001) [100]	0.08 (0.03) [0]
594 rpoB B1	<0.001 (<0.0001) [100]	0.07 (0.01) [0]
594 rpoB B8	0.01 (<0.0001) [78]	0.13 (0.03) [0]
594 rpoB C1	0.007 (0.10) [100]	0.36 (<0.0001) [0]
594 rpoB C4	0.003 (0.010) [0]	0.07 (<0.0001) [0]
594 rpoB C10	0.004 (0.001) [100]	1.00 (0.01) [0]
594 rpoB D2	0.38 (<0.0001) [0]	0.10 (<0.0001) [81]
594 rpoB D6	0.02 (0.01) [6]	0.03 (0.01) [86]

^a Plasmid includes precise sequence (ATG to TTC) for cII cloned into pcIpR-cII-timm in the same position in plasmid, relative to pR and the sR start site for rightward transcription as is gene cro in λWT, including its RBS sequence, except for substitution of a BamHI site cloning site incorporated into the RBS, eliminating the natural DNA sequence leftward (upstream) of cII, which includes a stem-loop structure [36] that could influence cII expression. The cII sequence in [cII] terminates with an ochre rather than TGA stop codon, Figure S1. ^b Plasmid includes the same sequence as in [cII] but with natural amber termination signal for cII, plus the natural partially cII-overlapping oop sequence, plus 94 nucleotides rightward of the start point (38685) for 5′ end of oop transcription, that includes the pO promoter for oop, through base 38769 in gene O. This encodes 28 amino acids from the N-terminal end of O, terminating with an inserted ochre stop codon, Figure S1 plasmids 2. ^c Data from Table 2 repeated here for comparison.