in contact with vancomycin (see figure 8C). Understanding this profile could be important for understanding vancomycin resistance, at least in SCO2594::Tn5062 mutant. We checked transcription of genes which could be implicated in vancomycin resistance, like for example; genes coding for sigma factors, penicillin-binding proteins, cell wall peptidoglycan biosynthesis enzymes (like [SCO3904] or genes femX mur or coding for a two component system involved in cell wall stress sensing cseBC, (Hong et al., 2002). The genes were not significantly regulated although they cseBC showed the same profile of and genes (see figure 8A); and the same happened whiB van with the only known target of WhiB in (Facey et al. 2011). In any S. coelicolor, dpsA case, only SCO1875, coding for a putative penicillin-binding protein, showed a significant regulation. This gene was more than two times up-regulated in the mutant strain. In a previous study, deletion of SCO1875 increased markedly vancomycin susceptibility in pointing to an important role of this penicillin-binding S. coelicolor; protein in glycopeptide resistance (Hesketh et al., 2011). The Pi cell wall content is highly reduced in the SCO2594::Tn5062 mutant According to Kleinschnitz and co-workers (2011), SCO2592 code for a B. subtilis homologue; being its function the glycosylation of teichoic acids. Moreover, the tagE transcription profile of SCO2592-94 resembles that of some teichoic acids B. subtilis genes (Liu et al., 1998). Therefore, we wondered if these genes could be implicated in the biosynthesis of any Pi polymer of the cell wall. To investigate this question parental and SCO2594::Tn5062 strains were cultured in the Pi-replete medium MG-18.5 and cell walls were isolated at the end of the exponential growth phase. The experiment clearly
in contact with vancomycin (see figure 8C). Understanding this profile could be important for understanding vancomycin resistance, at least in SCO2594::Tn5062 mutant. We checked transcription of genes which could be implicated in vancomycin resistance, like for example; genes coding for sigma factors, penicillin-binding proteins, cell wall peptidoglycan biosynthesis enzymes (like femX [SCO3904] or mur genes or cseBC, coding for a two component system involved in cell wall stress sensing (Hong et al., 2002). The cseBC genes were not significantly regulated although they showed the same profile of whiB and van genes (see figure 8A); and the same happened with the only known target of WhiB in S. coelicolor, dpsA (Facey et al. 2011). In any case, only SCO1875, coding for a putative penicillin-binding protein, showed a significant regulation. This gene was more than two times up-regulated in the mutant strain. In a previous study, deletion of SCO1875 increased markedly vancomycin susceptibility in S. coelicolor; pointing to an important role of this penicillin-binding protein in glycopeptide resistance (Hesketh et al., 2011). The Pi cell wall content is highly reduced in the SCO2594::Tn5062 mutant According to Kleinschnitz and co-workers (2011), SCO2592 code for a B. subtilis tagE homologue; being its function the glycosylation of teichoic acids. Moreover, the transcription profile of SCO2592-94 resembles that of some B. subtilis teichoic acids genes (Liu et al., 1998). Therefore, we wondered if these genes could be implicated in the biosynthesis of any Pi polymer of the cell wall. To investigate this question parental and SCO2594::Tn5062 strains were cultured in the Pi-replete medium MG-18.5 and cell walls were isolated at the end of the exponential growth phase. The experiment clearly
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