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Background  Secondary metabolism in  Serratia  sp. ATCC 39006 ( Serratia  39006) is controlled via a complex network of regulators, including a LuxIR-type (SmaIR) quorum sensing (QS) system. Here we investigate the molecular mechanism by which phosphate limitation controls biosynthesis of two antibiotic secondary metabolites, prodigiosin and carbapenem, in  Serratia  39006.    Results  We demonstrate that a mutation in the high affinity phosphate transporter  pstSCAB-phoU , believed to mimic low phosphate conditions, causes upregulation of secondary metabolism and QS in  Serratia  39006, via the PhoBR two-component system. Phosphate limitation also activated secondary metabolism and QS in  Serratia  39006. In addition, a  pstS  mutation resulted in upregulation of  rap . Rap, a putative SlyA/MarR-family transcriptional regulator, shares similarity with the global regulator RovA (regulator of virulence) from  Yersina  spp. and is an activator of secondary metabolism in  Serratia  39006. We demonstrate that expression of  rap ,  pigA-O  (encoding the prodigiosin biosynthetic operon) and  smaI  are controlled via PhoBR in  Serratia  39006.    Conclusion  Phosphate limitation regulates secondary metabolism in  Serratia  39006 via multiple inter-linked pathways, incorporating transcriptional control mediated by three important global regulators, PhoB, SmaR and Rap.

The PhoBR two-component system regulates antibiotic biosynthesis in Serratia in response to phosphate