The Rex phenotype is defined as the inability of T4rII mutant bacteriophage to form plaques on a lawn of E. coli lysogenized by bacteriophage lambda (λ), hence excluded (Rex). Although it has been more than five decades since the discovery of the Rex phenotype by Seymour Benzer in mid 1950s, the mechanism behind this legend is still mysterious.
The T4rII exclusion (Rex) system is encoded by two genes of λ (rexA, and rexB), the expression of which is primarily regulated by the repressor gene cI from the PM promoter. The onset of Rex, triggered by T4rII infection, results in rapid membrane depolarization and a harsh cellular environment that in many ways resembles stationary phase metabolism and morphology. In addition, disruption of the RexA:RexB balance can lead to the same Rex phenotypic manifestations without infection. Despite some cell killing, infected lysogens can recover from Rex activation. Rex may thus be a mutualistic protection mechanism that protects both itself and the host cell from external infection. We have designed a system for the rapid one-step isolation of host mutations that abrogate this phenotype, in order to identify the host genes involved in Rex and elucidate the mechanism of this enigmatic exclusion system.
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