Theories and methods developed in molecular pharmacology for drug receptor interactions were used to explain artificially induced myxospore formation. The correlation between inducer concentrations and the yield of myxospores, i.e. the experimentally obtained dose-response curves, were much steeper than expected for an interaction based on mass action law. We postulate that the interaction of an inducer with one of the different receptors of the bacterial cell causes the production of a common stimulus which programmes the cells to turn into myxospores, if a threshold value is reached. Simultaneous addition of inducers of the same or of different inducer groups showed synergistic interactions. Inducer concentrations that by themselves were not inducing gave maximum myxospore formation when combined. Addition of pyrrole, a specific inhibitor, caused a concentration-dependent parallel shift of the glycerol dose-response curve. Compounds, inducers or inhibitors, with identical receptor specificities competed for the common receptor according to their affinity. Interactions of inducers with different receptor specificities could be predicted from calculations with a mathematical model of functional synergism.


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