Suppression of λ PRM− mutations by cin-1, a mutation creating a new promoter for leftward transcription of the cl gene

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The cin-1 mutation, which was selected originally for its ability to suppress defects in the P RE pathway for λ repressor synthesis, also suppresses defects in the P RM pathway. Suppression of prm116, a prm − mutation, is manifest in the ability of λ c1857 prm116 cin-1 and λ c1857 prm116 cin-1 cII − to stably lysogenize Escherichia coli at 30–32° (isogenic cin + derivatives are unable to lysogenize). Radioimmune assays of repressor levels in lysogens indicate that λ c1857 prm116 cin-1 and λ c1857 prmll6 cin -l cII − prophages produce about 40–50% as much repressor as wild-type ( c1857) prophages. These and other results reported here support the idea that the cin-1 mutation creates a new promoter for leftward transcription of the cI (repressor) gene. Calculations based on the amount of repressor synthesized in lysogens containing a single prophage suggest that the cin-1 promoter may be significantly less active than the P RM promoter. On infection of sensitive cells at 30–32°, λ c1857 prm116 cin-1 cII68 and λ c1857 prm116 cin-1 produce low levels of repressor early, but by 60 min after infection the level of repressor is the same as that in cells infected with wild-type phage. This is probably due to the fact that cin-1-directed repressor synthesis is not subject to shutoff by λ cro protein.