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The T4rII exclusion (Rex) Phenotype is defined as the inability of rII mutants of bacteriophage T4 to generate plaques on a cell lawn of E. coli harboring a stably integrated lambda prophage. The selective exclusion of the rII mutants of T4 played a critical role in our understanding of modern molecular genetics. Shockingly, since first exploited by Seymour Benzer in the mid 1950's, the mechanism underpinning the Rex phenotype remains unexplained. T4rII exclusion is encoded by the lambda genes rexArexB coexpressed with the lambda repressor from the prophage as the PmcIrexArexBtimm operon. The onset of exclusion can result in the shutdown of cellular metabolism, preventing the replication of the superinfecting T4rII bacteriophage. In addition to reviewing the historic plight to characterize and resolve the Rex phenotype, we tackle this enigmatic phenomenon, adding important pieces to this puzzle and offer a working model for the mechanism of action.
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birth defects, or other reproductive harm.
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