The ribosome inhibitor chloramphenicol brings about a rapid disappearance of ppGpp in both RC+ and RC- cells, suggesting that the antibiotic inhibits the synthesis of ppGpp. The kinetics of ppGpp decay in the presence of chloramphenicol agrees well with the kinetics of ppGpp accumulation, in the antibiotic's absence, both in RC+ cells subjected to amino acid starvation and in RC- cells subjected to carbon source downshift. In the latter case, a reduction in the rate of ppGpp degradation accounts for the accumulation of ppGpp. Thus, although RC- mutants cannot adjust the rate of ppGpp synthesis in response to amino acid starvation, they retain the ability to adjust the rate of ppGpp degradation in response to carbon source downshift. The latter control mechanism may account for the fact that the ppGpp level during balanced growth varies, in both RC+ and RC- cells, from one growth medium to another in relation to the growth rate which the medium will support. The fact that chloramphenicol inhibits ppGpp formation in RC- as well as RC+ cells suggests, for reasons discussed, that the antibiotic inhibits ppGpp synthesis directly.
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Gallant et al. (1972) studied this question.
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