DISSOCIATION OF MACROMOLECULAR SYNTHETIC PROCESSES IN T2-INFECTED E. COLI

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Abstract
The foregoing observations lead us to conclude that the inhibitory action of FUdR on T2 bacteriophage production is a block in the de novo synthesis of DNA as expected, and an inhibition of the conversion of bacterial DNA to T2 DNA by a mechanism not presently known. We ascribe the absence of phage production in singly infected cells, compared to the low, but definite, phage yield obtained from multiply infected cells, to the following series of events. Parental T2 DNA undergoes fragmentation after entering the host. Replication of intact DNA is virtually eliminated by FUdR. In multiply infected cells, repair of DNA can be made by utilization of a pool of parental DNA fragments, or subunits, adequate for the re-formation of only one to three complete DNA molecules. The possibility exists that replacement of some nucleotides deleted by hydrolysis must occur prior to the joining of such subunits. The observation that T2-specific RNA and protein are synthesized at a reasonably normal rate in the virtual absence of DNA synthesis strongly suggests that the DNA template (s) for the synthesis of DNA-like RNA are stable and do not have to undergo continued renewal. The protein, synthesized together with T2 -specific RNA or synthesized subsequent to the accumulation of T2-specific RNA, seems to be of a normal composition. Part of the T2 structural protein accumulated in the absence of T2 DNA synthesis can be quickly incorporated into mature phage particles with the onset of DNA synthesis. The molecular nature of the usable protein remains a subject under current investigation. The data confirm our previous conclusion that T2-specific RNA is not a stable catalyst.