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Upon infecting populations of susceptible host cells, T-even bacteriophages maximize their yield by switching from lysis at about 25 to 35 min at 37°C after infection by a single phage particle to long-delayed lysis (lysis inhibition) under conditions of sequential infection occurring when free phages outnumber host cells. The timing of lysis depends upon genet and upon one or more rapid-lysis (r ) genes whose inactivation prevents lysis inhibition.t encodes a holin that mediates the movement of the T4 endolysin though the inner cell membrane to its target, the cell wall. The rI protein has been proposed to sense superinfection. Of the five reasonably well characterizedr genes, only two,rI andrV , are clearly obligatory for lysis inhibition. We show here thatrV mutations are alleles oft that probably render the t protein unable to respond to the lysis inhibition signal. Thetr alleles cluster in the 5′ third oft and produce a strong r phenotype, whereas conditional-lethalt alleles produce the classical t phenotype (inability to lyse) and othert alleles produce additional, still poorly understood phenotypes.tr mutations are dominant tot + , a result that suggests specific ways to probe T4 holin function.

Lysis and Lysis Inhibition in Bacteriophage T4: rV Mutations Reside in the Holin t Gene