Lysis and lysis inhibition in bacteriophage T4: rV mutations reside in theholin t gene

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 d egrees C after infection by a single phage particle to long-delayed lysis ( lysis inhibition) under conditions of sequential infection occurring when f ree phages outnumber host cells. The timing of lysis depends upon gene t an d upon one or more rapid-lysis (r) genes whose inactivation prevents lysis inhibition. t encodes a holin that mediates the movement of the T4 endolysi n though the inner cell membrane to its target, the cell wall. The rI prote in has been proposed to sense superinfection, Of the five reasonably well c haracterized r genes, only two, rI and rV, are clearly obligatory for lysis inhibition. We show here that rV mutations are alleles oft that probably r ender the t protein unable to respond to the lysis inhibition signal. The t r alleles cluster in the 5' third of t and produce a strong r phenotype, wh ereas conditional-lethal t alleles produce the classical t phenotype (inabi lity to lyse) and other t alleles produce additional, still poorly understo od phenotypes. tr mutations are dominant to t(+), a result that suggests sp ecific ways to probe T4 holin function.