| Abstract [eng] |
Bacteriophage PRD1 from Tectiviridae family uses its internal membrane to enter the host multiple resistant to antibiotics Gram-negative bacteria. Some indirect evidences indicate that during the entry phage membrane fuses with the plasma membrane of bacterial cell. However, it is very complicated to get the direct evidences or indications of the membrane fusion in this system. Monitoring the phage-induced fluxes of TPP+ and K+ ions and studying the influence of membrane-active antibiotics on membrane voltage and potassium gradient we were investigating PRD1-induced changes in the permeability of the outer and the plasma membranes of Salmonella enterica cells and registering the influence of physicochemical parameters of infection medium on the efficiency of phage-cell interaction. We have shown that phage PRD1 increases permeability of the outer membrane but does not depolarize the plasma membrane during the entry. 300 OsmM and higher osmotic pressure in the infection medium and temperature lower than 22 oC blocks the phage induced changes in bacterial envelope. Differently from the relative bacteriophage Bam35, divalent cations are not needed for PRD1 entry. Complexones of divalent cations EDTA and EGTA stimulate, but Ca2+ ir Mg2+ slightly inhibit the plasma membrane-permeabilizing activity of PRD1. Arsenate inhibits PRD1 induced changes of the cell envelope and the reduced intracellular ATP content could be the reason. Bacteriophage-induced lysis of S. enterica cells is aeration-dependent and the shortest infection cycle was observed at conditions of intensive aeration. Arsenate stimulated but divalent cations had no effect on the lysis of PRD1 infected cells. |
