Sudden nutritional deprivation, or starvation, insists that the bulk energy demands for replication, transcription, and translation cannot be met by the current conditions. Amino acid starvation induces the “stringent response” in many prokaryotic organisms, which is a means to adapt to the unfavorable conditions. Signaling of the stringent response is accomplished with the synthesis of two guanine nucleotides, pppGpp and ppGpp. Examination of DNA content by flow cytometry is employed to investigate the replication arrest profile of stringent E. coli cells. The results indicate that cells reversibly arrest in their B period with cohesion at the chromosomal termini. Furthermore, the pattern of DNA methylation and the binding of the protein SeqA to the DNA are necessary to enforce this arrest. Changes in transcription, induced by the direct binding of ppGpp to RNAP, are necessary for the replication arrest as well. The conserved bacterial G-protein, ObgE, also regulates this arrest through ppGpp binding. Induction of the stringent response is a useful means of synchronizing cells for DNA replication. A (p)ppGpp-dependent change in nucleoid morphology is also apparent after stringent induction. Specifically, a single helical-like DNA mass extends across the cell length, reminiscent of the MreB filament after starvation. Stringent transcription influences this morphology, and the architectural proteins H-NS and Fis do not. Decondensation of the nucleoid is likely an active process, since it can overcome topological constraints induced by H-NS overproduction. In general, dramatic alterations in the E. coli cell are induced by (p)ppGpp. The features of active growth: replication, cell division, chromosome segregation, DNA condensation, transcription, and translation, are all inhibited by (p)ppGpp. Moreover, several elements that regulate active growth overlap with those that govern (p)ppGpp-mediated growth inhibition.