The rexA and rexB genes of bacteriophage A. encode a two-component system that aborts lytic growth of bacterial viruses. Rex exclusion is characterized by termination of macromolecular synthesis, loss of active transport, the hydrolysis of ATP, and cell death. By analogy to colicins El and K, these results can be explained by depolarization of the cytoplasmic membrane. We have fractionated cells to determine the intracellular location of the RexB protein and made RexB-alkaline phosphatase fusions to analyze its membrane topology. The RexB protein appears to be a polytopic transmembrane protein. We suggest that RexB proteins form ion channels that, in response to lytic growth of bacteriophages, depolarize the cytoplasmic membrane. The Rex system requires a mechanism to prevent X itself from being excluded during lytic growth. We have determined that overexpression of RexB in A. lysogens prevents the exclusion of both T4 rll mutants and X ren mutants. We suspect that overexpression of RexB is the basis for preventing self-exclusion following the induction of a \ lysogen and that RexB overexpression is accomplished through transcriptional regulation.