Control Mechanisms in T4 Infection: Studies on the Exclusion of the RNA Phage M12 in Mixedly Infected Cells

Abstract

It is well known that following infection of E. coli cells with phages of the T-even class (T2, T4, T6) the macromolecular syntheses of the host cell are rapidly stopped (Cohen, 1947, 1948; Volkin and Astrachan, 1956; Nomura, Hall and Spiegelman, 1960). In an attempt to elucidate the mechanism by which T-even phage controls RNA and protein-synthesis determined by genetic elements other than its own, the exclusion of RNA phage M12 was studied in cells mixedly infected with phage T4. In particular, the following points were examined: (1) The possible interference of T4 infection with M12 penetration, (2) the intracellular fate of parental M12 RNA, (3) the synthesis of replicative intermediates and single-stranded progeny RNA, (4) the formation of defective phage particles and (5) the production of phage coat protein. Results of these experiments suggested that T4 may specifically interfere with the mRNA function of the M12 chromosome. In a second series of experiments this hypothesis was further strengthened by studying the formation of M12 specific polysomes and RNA polymerase. In mixed infections the production of RNA polymerase is completely blocked, but the formation of polysomes containing parental M12 RNA is normal. These findings are interpreted to mean that T4 interferes with translation of the M12 RNA, possibly on the polysomal level.