Abstract

Polyphosphate, which is synthesized by the enzyme polyP kinase (PPK), is an important energy and phosphate storage polymer that plays a crucial role in the regulation of adaptive responses of cells to physical and chemical stresses. In this work, the polyphosphate kinase gene (ppk) of Streptomyces coelicolor was deleted, and the effect of this mutation on actinorhodin and undecylprodigiosin biosynthesis was investigated. Deletion of the ppk gene had a stimulatory effect on actinorhodin production; the mutant strain produced about 5 times more antibiotic compared to the wild type strain at 120 h of growth. There was no difference in undecylprodigiosin production between the mutant and wild-type strains. In the presence of a selective antibiotic, the mutant strain could grow only on rich medium and could not sporulate effectively. Moreover, while the wild type strain was resistant, the mutant strain was sensitive to H_2O_2 in the conditions tested. Mutant characters were complemented by the ppk gene, which is cloned on a high copy number plasmid.

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