Inhibtory effect of colicin E2 on transport systems of Escherichia coli in the presence of the rex gene of lambda prophage.

Abstract

Purified colicin E(2) was found to cause marked inhibition of the permeation rate of o-nitrophenyl-galactoside (ONPG) in several lambda-lysogenic strains of Escherichia coli in the presence of chloramphenicol to prevent prophage induction. The inhibitory effect of colicin E(2) on transport systems was analyzed with cells of E. coli CP78(lambda). The dose of colicin E(2) for the half-maximum inhibition of the ONPG-permeation rate was about 9 molecules of the colicin per bacterium under the aerobic condition, which corresponded to about 1 killing unit per bacterium. Kinetics of the transport of [(14)C]methylthiogalactoside suggested that colicin E(2) began to inhibit the influx rate of beta-galactosides within a few minutes after the colicin addition, and the maximum inhibition reached more than 80%. Extensive leakage of intracellular potassium ion and inhibition of l-proline transport also occurred at the same time. Acid solubilization of cellular deoxyribonucleic acid by the colicin was apparently delayed to the initiation of the transport inhibition. The extents of the inhibition of beta-galactoside transport and leakage of potassium ion by the colicin were extensive in cells lysogenic for wild lambda phage or lambdaind(-), whereas the extents were slight in the nonlysogenic cells or cells carrying lambdarex(-) prophage. It was concluded that the sensitization of membrane transport systems of E. coli cells to colicin E(2) was achieved by the presence of the rex gene product of lambda phage.