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- W1998184145 abstract "Previously reported experiments show that λc17 replicates constitutively when it infects an immune host but that phage carrying c17 do not produce lysis of the immune host with liberation of new virus (virulence) unless they also carry a cI mutation. A model presented to explain λc17cI virulence proposed that (i) although some genes in λ carrying c17 operate constitutively, others are still subject to cI+-represser in the immune host, (ii) the repressed genes are derepressed if constitutive replication produces too many λ copies for the cI+-repressor to control, and (iii) this occurs only if the replicating element is unable to augment the level of represser produced by the prophage. In other words, it was proposed that λc17cI is virulent because its constitutive replication leads to oversaturation of the cI+ repressor produced by the prophage and this leads to expression of genes which were initially subject to repression in the input λc17cI. Experiments of two types are presented which support this interpretation. First, studies of the expression of the N-controlled gene specifying λ exonuclease show that (i) this gene is subject to repression in phage carrying c17, (ii) this gene is eventually derepressed following infection with phage carrying both c17 and a cI mutation, and (iii) this derepression is blocked if the λc17cI carries a third mutation which blocks its replication. A second set of experiments also supports the model by showing that increasing the number of cI+ genes capable of forming repressor delays or prevents lysis of the immune host by λc17cI, presumably by augmenting the cI+-repressor produced by the prophage sufficiently to delay, and in some cells even prevent, oversaturation of the cI+ -repressor by λc17cI copies." @default.
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- W1998184145 date "1969-06-01" @default.
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- W1998184145 title "Mechanism of λc17cI virulence" @default.
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- W1998184145 doi "https://doi.org/10.1016/0022-2836(69)90231-9" @default.
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