Permeability lesions in male Escherichia coli infected with bacteriophage T7.

Abstract

The abortive development of bacteriophage T7 in E. coli cells carrying F factors has previously been attributed to a lack of virus-directed modification of ribosomes in such cells. We find it unnecessary to postulate such translational control to explain the failure of T7 development. Instead, there is a general cessation of macromolecular syntheses around 8 min after T7 infection of F' cells. This cessation is correlated with a sudden outflow of the entire acid-soluble pool of phosphorus-containing compounds and loss of the ability to accumulate amino acids. Manifestation of these defects requires expression of at least one T7 gene and one episomal gene.