A pleiotropic mutation (cpm) which is localized in the vicinity of the spoOA gene is described in Bacillus subtilis. The mutation inhibits spore formation, rendering bacteria auxotrophic for adenine and tyrosine, enhances sensitivity to antibiotics, decreases cell motility, inhibits the ability to grow on pentoses and to maintain bacteriophage multiplication, induces severalfold the activities of alkaline proteinase and alpha-amylase. At the same time, the cpm mutant starts to excrete inosine into the growth medium. This excretion most probably is explained by a 50-fold increase in the activity of inosine monophosphate: 5'-nucleotidase and a 10-fold decrease in the activity of purine nucleoside phosphorylase. The inosine production and Ade- phenotype of the cpm mutant is not accompanied by the change in the activity of succinyl adenosine monophosphate synthetase. The nature of the mutation is discussed.

A pleiotropic mutation (cpm) which is localized in the vicinity of the spoOA gene is described in Bacillus subtilis. The mutation inhibits spore formation, rendering bacteria auxotrophic for adenine and tyrosine, enhances sensitivity to antibodiotics, decreases cell motility, inhibits the ability to grow on pentoses and to maintain bacteriophage multiplication, induces severalfold the activities of alkaline proteinase and α‐amylase. At the same time, the cpm mutant starts to excrete inosine into the growth medium. This excretion most probably is explained by 1 50‐fold increase in the activity of inosine monophosphate: 5′‐nucleotidase and a 10‐fold decrease in the activity of purine nucleoside phosphorylase. The inosine production and Ade− phenotype of the cpm mutant is not accompanied by the change in the activity of succinyl adenosine monophosphate synthetase. The nature of the mutation is discussed.