Abstract

Under normal conditions, phage T4-infected bacteria lyse at a characteristic time after infection, each infected cell releasing a few hundred progeny phage. To investigate the mechanism of this lysis, a selection technique was used to isolate lysis-defective mutants of phage T4. A new class of lysis-defective mutants was found which define a new T4 gene called t. During infection, t-defective mutants synthesize both phage and phage lysozyme, yet fail to either cease metabolism or lyse at the usual time. Thus, T4-induced lysis entails a sequence of at least two events: function of t gene product, resulting in the cessation of host metabolism and allowing e gene product, phage lysozyme, to degrade the host cell wall and release progeny phage. Although the mechanism of T4 t gene product remains to be determined, some alternatives were ruled out. Neither a metabolic poison nor exogenous lysozyme will phenotypically revert the t gene defect. These results show that the normal function of gene t involves something besides cessation of host metabolism and disruption of the host cell wall. To test whether t gene product acts by degrading host membrane phospholipid, hydrolysis of host phospholipid was measured during T4 infection. It was found that lysis, although normally accompanied by phospholipid hydrolysis, can occur in the absence of this reaction. Thus the phospholipid hydrolysis observed is a by-product of the t gene event rather that a requirement for lysis. The role of gene t in the lysis mechanism of phage T4 is discussed in light of these results.

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