Changes in host cell energetics in response to bacteriophage PRD1 DNA entry

Double-stranded DNA bacteriophage PRD1 infects a variety of gram-negative bacteria harboring an IncP-type conjugative plasmid. The plasmid codes for the DNA transfer phage receptor complex in the cell envelope. Our goal was, by using a collection of mutant phage particles for which the variables are the DNA content and/or the presence of the receptor-binding protein, to obtain information on the energy requirements for DNA entry as well as on alterations in the cellular energetics taking place during the first stages of infection. We studied the fluxes of tetraphenylphosphonium (TPP1), phenyldicarbaundecaborane (PCB2), and K1 ions as well as ATP through the envelope of Salmonella typhimurium cells. The final level of the membrane voltage (DC) indicator TPP1 accumulated by the infected cells exceeds the initial level before the infection. Besides the effects on TPP1 accumulation, PRD1 induces the leakage of ATP and K1 from the cytosol. All these events were induced only by DNA-containing infectious particles and were cellular ATP and DC dependent. PRD1-caused changes in DC and in PCB2 binding differ considerably from those observed in other bacteriophage infections studied. These results are in accordance with the presence of a specific channel engaged in phage PRD1 DNA transport. PRD1 is a double-stranded DNA bacterial virus. The virion is composed of an outer protein coat which surrounds th