Abstract
Nonlysogenic Escherichia coli K cells exhibit a delay in lysis when infected by T4 rII phage termed lysis inhibition (LIN). E. coli K cells expressing λ rexB from either a prophage defective for rexA, or a multicopy plasmid supported T4 rII infection, but prevented the establishment of LIN. In addition, E. coli null mutations in either the periplasmic “tail-specific protease” tsp, or the 10Sa RNA ssrA, completely blocked the establishment of LIN following T4 infections. The expression of rexB in the absence of rexA resulted in several cellular phenotypes, including aberrant cell surface morphology, the partial to near complete suppression of mutations of λ S and T4 t holin genes, and lysis by cells aging on plates or growing with high rexB expression at elevated temperatures. These activities of RexB were impeded in the presence of RexA.
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