The effect of phosphate deficiency on quorum sensing signaling pathway of Sinorhizobium meliloti

Phosphorus is one of the most essential macroelements for bacterial cells. Since phosphate (PO4-3) limitation is frequently encountered in soils, bacteria developed some mechanisms in response to this sever condition. Phosphate transporter (PstS) and proteins involved in quorum sensing (QS) signaling pathway are affected by mediating PhoB, response regulator, following phosphate starvation. QS system of Sinorhizobium meliloti composed of at least three genes of sinI (autoinducer synthase), sinR and expR (autoinducer activated receptor) which involved in its free living and symbiotic functions. The optical density (OD600) of different S. meliloti transformed strains carrying pLK004 (a pstS promoter-egfp fusion), pLK64 (a sinI promoter-egfp fusion), pLK65 (a sinR promoter-egfp fusion), pLK66 (an expR promoter-egfp fusion) and control (promoterless-egfp fusion) plasmids were read under different phosphate concentrations of 0.1 (phosphate deficiency), 0.5 and 2 mM (sufficient phosphate) at several time points of 16, 24 and 40h. The promoter activity of different genes of pstS, sinI, sinR and expR were measured as emitted fluorescence per bacterial cell density (OD600) under different phosphate concentrations. By reducing phosphate concentration in the medium, the growth rate of transformed bacteria decreased, especially at 40h. The promoter activity of pstS, sinI and sinR, but not expR, genes was activated following phosphate starvation. Discussion and S. meliloti can upregulate PstS to partly compensate phosphate deficiency in the environment. The gene of sinR is also activated in a PhoB dependent manner as phosphate starvation is encountered. SinR is the activator of sinI, so the upregulation of QS pathway under phosphate deficiency may be facilitate free living and symbiotic bacterial functions.