Physiological studies on the t gene defect in T4-infected Escherichia coli

Abstract

Su − bacteria infected with T4 phage carrying an amber mutation in gene t synthesize both phage and phage lysozyme, yet fail to either cease metabolism or lyse at the usual time ( Josslin, 1970). The experiments reported in this paper show that (1) addition of egg white lysozyme allows a normal lysis of cells infected with lysozyme-defective mutant phage but does not significantly affect the lysis phenotype of cells infected with t mutant phage; (2) anaerobiosis or addition of cyanide induces infected cell lysis only if the t gene is functional; (3) mutations in the rII genes partially suppress the lysis-defective, t mutant phenotype; (4) revertants of t mutant phage are often double mutants carrying the original t mutation as well as a mutation in either of the two rII genes or, less frequently, at a site not closely linked to rII. The first two observations show that the t gene defect cannot be overcome simply by artificially disrupting the cell wall or inhibiting metabolism. They are consistent with the hypothesis that the t gene product induces the disruption of the cell membrane, which causes cessation of host metabolism and allows the e gene product to initiate digestion of the cell wall.