Abstract Background: Vancomycin is an essential antibiotic to treat infections caused by multiple-drug bacteria such as methicillin-resistant (MRSA), a major Staphylococcus aureus killer in hospital-acquired infections. Vancomycin-resistant phenotypes were first reported in enterococci in 1987 and later spread to important pathogens like MRSA. Hong and coworkers reported in the first example of Streptomyces coelicolor vancomycin resistance in a nonpathogenic and non-glycopeptide-producing bacterium. Later, we showed that vancomycin resistance in depends on the phosphate S. coelicolor concentration of the culture medium. Actually, phosphate concentrations higher than 0.5 % decreased more than four times the minimum inhibitory concentration values of vancomycin on MMCGT medium. In this study, we discuss the vancomycin-resistant phenotype of a disrupted mutant which is highly resistant to vancomycin S. coelicolor under high phosphate concentrations. Results: Whilst screening for phenotypes of PhoP-regulated genes without a previously assigned function, we have identified a disrupted mutant (SCO2594::Tn5062) S. coelicolor lacking the phosphate control of vancomycin resistance that the parental strain exhibits. In order to understand the regulatory pathways that produce this phosphate-dependent vancomycin resistance phenotype we have performed a transcriptomic analysis using S. parental and SCO2594::Tn5062 mutant strains. Several proteins seem to be coelicolor implicated in this regulatory mechanism including different regulators, sigma factors,
Abstract Background: Vancomycin is an essential antibiotic to treat infections caused by multiple-drug bacteria such as methicillin-resistant Staphylococcus aureus (MRSA), a major killer in hospital-acquired infections. Vancomycin-resistant phenotypes were first reported in enterococci in 1987 and later spread to important pathogens like MRSA. Hong and coworkers reported in Streptomyces coelicolor the first example of vancomycin resistance in a nonpathogenic and non-glycopeptide-producing bacterium. Later, we showed that vancomycin resistance in S. coelicolor depends on the phosphate concentration of the culture medium. Actually, phosphate concentrations higher than 0.5 % decreased more than four times the minimum inhibitory concentration values of vancomycin on MMCGT medium. In this study, we discuss the vancomycin-resistant phenotype of a S. coelicolor disrupted mutant which is highly resistant to vancomycin under high phosphate concentrations. Results: Whilst screening for phenotypes of PhoP-regulated genes without a previously assigned function, we have identified a S. coelicolor disrupted mutant (SCO2594::Tn5062) lacking the phosphate control of vancomycin resistance that the parental strain exhibits. In order to understand the regulatory pathways that produce this phosphate-dependent vancomycin resistance phenotype we have performed a transcriptomic analysis using S. coelicolor parental and SCO2594::Tn5062 mutant strains. Several proteins seem to be implicated in this regulatory mechanism including different regulators, sigma factors,