Sporulation in the prokaryotic Bacillus subtilis can be initiated by partial deprivation of amino acids, which causes a "stringent response". Certain antibiotics prevent this induction with almost no inhibition of growth. Their effect was counteracted by decoyinine which specifically inhibits the synthesis of guanosine monophosphate (GMP). The stringent response also inhibits the uptake of guanine and uracil, but only the latter is also inhibited by addition of decoyinine alone. Thus, the increase of ppGpp controls some reactions directly and others indirectly, via the decrease of GTP. To understand the mechanisms controlling the synthesis of a typical developmental protein, the gene for glucose dehydrogenase of B. subtilis was cloned. In the non-differentiating E. coli, the plasmid caused production of active glucose dehydrogenase during vegetative growth. However, a low copy plasmid shuttle vector produced essentially no glucose dehydrogenase activity in B. subtilis, and a high copy plasmid produced a low amount of enzyme; this suggests the titration of a repressor. In vitro, the gene could be transcribed into RNA, but only by a minor component of RNA-polymerase of B. subtilis which may play a special developmental role. The relevant DNA has been sequenced. The cell wall turnover deficiency of B. subtilis lyt mutants was found not to be due to the lack of peptidoglycan hydrolases as previously claimed by others. Turnover deficiency in one of these strains (lyt-l5) can be prevented by 0.2 M NaCl (other cations are less effective) and is due to a yet unidentified change in the wall. Sporulation of a rodB strain, which grows as a rod at 30 C and as a sphere at 45 C, was at 45 C unable to form a prespore septum. This suggests that the topological information provided by the cell shape is required for sporulation.