Effects of temperature and host cell genetic characteristics on the replication of the lipid-containing bacteriophage PR4 in Escherichia coli

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Abstract
The lipid-containing bacteriophage PR4 is of special interest, for it can replicate in various gram-negative bacteria, including E. coli, that carry one of a group of drug resistance plasmids. PR4 grown in E. coli strain PS2R contains .apprx. 10% lipid by weight, with the negatively charged phospholipid phosphatidylglycerol being the most abundant lipid in the virion. PR4 attaches to E. coli with an attachment rate constant of Ka .apprxeq. 6.2 .times. 10-10 ml/min, which is about twice that of the enveloped phage .phi.6 (to Pseudomonas phaseolicola), but a factor of 5 less than that of phage PM2 (to Pseudomonas BAL-31). Use of an E. coli glycerol auxotroph indicated that a normal amount of PR4 replication occurs only if glycerol starvation (inhibition of all phospholipid synthesis) begins no earlier than about halfway through the lytic cycle. Use of an E. coli fatty acid synthesis temperature-sensitive [ts] mutant and an E. coli phosphatidylethanolamine synthesis ts mutant indicated that PR4 replication can occur in the absence of normal fatty acid synthesis or normal phospholipid synthesis if the infection takes place prior to the termination of overall cell growth and the onset of cell death. The PR4 burst size in nutrient media at 30-42.degree. C is .apprx. 40, but the burst size at 20.degree. C is < 3. Temperature-shift experiments show that the temperature late in infection determines the burst size.