Abstract

The effect of chloramphenicol on RNA turnover in T2-infected E. coli was studied with the aid of 32P-labeled orthophosphate. When chloramphenicol is added before infection, the subsequent distribution of radioactivity among RNA mononucleotides is different from the distribution found in control infected cells and resembles the distribution found in uninfected cells. When chloramphenicol is added after infection, the 32P distribution in RNA is that typical of infected cells. If the infected cells are inhibited before or shortly after infection, RNA turnover and DNA synthesis are inhibited. When chloramphenicol is added 9 min after infection, conditions that allow DNA synthesis, the rate of 32P incorporation into RNA is increased and turnover of RNA now occurs in the presence of chloramphenicol. Thus RNA turnover is blocked under conditions that prevent DNA synthesis, but RNA turnover is not inhibited when DNA synthesis can proceed. These observations are in agreement with the concept that some protein synthesis must precede or accompany formation of an RNA peculiar to phage-infected bacteria. It is also suggested that in the presence of inhibitor, RNA is synthesized by reversible reactions from precursor material also used for DNA synthesis.

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