Glucose kinase alone cannot be responsible for carbon source regulation in Streptomyces peucetius var. caesius.

Using an antibiotic enrichment procedure, eight mutants of Streptomyces peucetius var. caesius were isolated for their sensitivity to the glucose analogue 2-deoxyglucose (DOG), from a DOG-resistant strain (Dog(R)). These mutants (Dog(S)) and their parent strain were examined for growth sensitivity to DOG, glucose kinase (Glk) activity, glucose uptake, and sensitivity to repression by glucose and other catabolites derived from it. No correlation was found between Glk levels or glucose uptake and carbon catabolite repression (CCR) in these strains. However, the ratio of glucose uptake to Glk activity, and thus the flux through glycolysis, seemed responsible for this effect. Among several products of glucose catabolism tested, fructose-1,6-bis-phosphate and phosphoenolpyruvate showed significant repression of anthracycline formation. These compounds also reduced anthracycline formation in a Dog(R) mutant insensitive to glucose repression. Our data suggest that Glk alone is not sufficient to elicit CCR in this microorganism, and gives the first physiological evidence supporting the hypothesis that some products of glucose catabolism are involved in CCR in Streptomyces.