The metabolism of ribonucleic acid in normal and bacteriophage infected Escherichia coli.

Cohen (1948a) has reported that during the multiplication of the bacteriophages T2r+ and T4r+ in Escherichia coli, strain B, the ribonucleic acid content of the host remains constant. Similar observations were made by Kozloff et al. (1951) who investigated the origin of the nitrogen of T6r+ multiplying in the same host. Cohen (1948b) also examined the possibility that the ribonucleic acid was undergoing turnover during T2r+ multiplication. Using the incorporation of inorganic p32 into the ribonucleic acid as an indicator of such a turnover, he found that almost no p32 was incorporated into the ribonucleic acid. In a recent paper by Koch et al. (1952) these authors state in a footnote that "purines, like phosphorus, do not turn over in the RNA of the infected cell". The apparent inertness of the ribonucleic acid of the infected cell might be explained in several ways: (1) It is possible that in the growing host the enzymatic pathway leading from precursors such as glycine and inorganic phosphate to ribonucleic acid is a reversible one and accordingly in a state of dynamic equilibrium. If this is the case, isotopic precursors could be incorporated into the ribonucleic acid without a net increase of the ribonucleic acid. Incorporation of isotope by such a mechanism could be termed "incorporation by exchange". To explain the lack of incorporation of isotope into the ribonucleic acid during phage infection, one would have to postulate that there is an inhibition during phage infection of one or more of the enzymes in this pathway, preventing incorporation of isotope into the ribonucleic acid. (2) Synthesis and degradation of the ribonucleic acid of the growing cell could be taking place by different enzymatic pathways, both essentially irreversible. In this case, isotope could be incorporated into the