Abstract

Abstract The requirement for T4 gene 57 function, normally essential for tail fiber assembly and phage production, can be partially bypassed in mutants of host E. coli strains B and K12 ( byp mutants). 57 − Mutants plate with almost full efficiency on the byp hosts, but burst sizes in liquid culture are only 10% of normal, and tail fiber antigen production is also subnormal. The byp mutations are specifically permissive for 57 − mutant phage; amber mutants defective in other genes do not grow on the byp hosts. Enhanced 57 − phage growth reflects an increased rate of intracellular phage production rather than an extended latent period. The mutation in one byp strain, BP4, affects cell growth, cell morphology, and T4 rII plaque morphology in addition to the growth of 57 − phage. Simultaneous reversion of all these mutant characteristics suggests a single mutational origin. The nature of host byp mutations is discussed in relation to the possible mechanism of gene 57 function in normal T4 development.

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