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Appl Environ Microbiol. 1994 March; 60(3): 785-791
Copyright © 1994, American Society for Microbiology. All Rights Reserved.

Production of Bacteriolytic Enzymes by Streptomyces globisporus Regulated by Exogenous Bacterial Cell Walls

Institut für Genetik und Mikrobiologie der Universität München, 80638 Munich, Germany

ABSTRACT

Mutanolysin biosynthesis and pigment production in Streptomyces globisporus ATCC 21553 were stimulated by adding bacterial cell walls to the medium. The increased bacteriolytic activity in the supernatant correlated with an increased de novo synthesis of mutanolysin and was between 4- and 20-fold higher than in cultures grown without bacterial cell walls. The increase in mutanolysin synthesis was brought about by enhanced transcription of the mutanolysin gene. The stimulation was only observed in medium which contained dextrin or starch as the carbon source. Glucose abolished the stimulation and also inhibited the low constitutive synthesis of mutanolysin. The induction of lytic activity was observed to require minimally 0.4 mg of bacterial cell walls per ml, whereas 0.6 mg of bacterial cell walls per ml yielded maximal lytic activity. Further supplements of bacterial cell walls did not result in enhanced lytic activity. The stimulation could be achieved independently of the phase of growth of the Streptomyces strain. Cultures grown in the presence of bacterial cell walls exhibited a higher growth yield. However, the accelerated growth was not the reason for the increased amount of mutanolysin produced. The growth of cultures with peptidoglycan monomers added to the medium instead of cell walls was similarly increased, but an effect on the biosynthesis of mutanolysin was not observed. All bacterial cell walls tested were capable of eliciting the stimulation of lytic activity, including cell walls of archaea, which contained pseudomurein.

^* Corresponding author. Mailing address: Institut für Genetik und Mikrobiologie der Universität München, Maria-Ward-Str. 1a, 80638 Munich, Germany. Phone: (089) 17919852. Fax: (089) 17919849.