Increased synthesis of an Escherichia coli membrane protein suppresses F exclusion of bacteriophage T7.

Increased synthesis of the protein FxsA alleviates the exclusion of T7 in cells harboring the F plasmid. In contrast to wild-type or cells defective in fxsA, overexpression of fxsA+ allows T7 to form plaques at normal efficiency even though the burst size is reduced to about half that obtained on the isogenic F- strain. No defect in DNA synthesis was observed but late protein synthesis remains partially inhibited and a reduced level of cell leakiness, a prominent feature of F+ cells abortively infected by T7, persists. The FxsA protein is shown to be a cytoplasmic membrane protein. How T7 avoids exclusion by F in cells that exhibit increased levels of FxsA is discussed in terms of its membrane localization.

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