Reduction of colicin E2-induced DNA breakdown by the rex gene of λ prophage

Saxe, Linda S

doi:10.1016/0042-6822(74)90387-0

Cited by 7 publications

(5 citation statements)

References 13 publications

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“…It is not known whether colicin E2 penetrates cells. It is less effective against X-lysogens; the product of the rex gene, which is known to affect the membrane in lysogens infected with T4rII or Ti, is responsible (498). Similarly, the protection conferred by OX174, even when inactivated by UV, may result from alterations of the envelope produced by the bacteriophage (508).…”

Section: Action Of Colicins E3-ca38 and E2-p9mentioning

confidence: 99%

Colicinogeny and related phenomena.

Hardy¹

1975

Bacteriological Reviews

130

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Section: Action Of Colicins E3-ca38 and E2-p9mentioning

confidence: 99%

Colicinogeny and related phenomena.

Hardy¹

1975

Bacteriological Reviews

130

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“…Bacteriophage X has been found to confer the capacity on the lysogenic cells to block the multiplication ofrII mutants of T4 phage, which mainly involves the product of the rex gene of X (12,15). Observations had been made that 618 BEPPU, YAMAMOTO, AND ARIMA acid solubilization of DNA by colicin E2 was partially reduced at late times of the colicin challenge in cells carrying X prophage (16,20), and this reduction was due to the rex gene product (23). This effect may be elucidated by the marked inhibition of membrane transport systems observed here.…”

mentioning

confidence: 99%

Inhibitory Effect of Colicin E ₂ on Transport Systems of Escherichia coli in the Presence of the rex Gene of λ Prophage

Beppu

Yamamoto

Arima

1975

Antimicrob Agents Chemother

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Purified colicin E2 was found to cause marked inhibition of the permeation rate of o-nitrophenyl-galactoside (ONPG) in several X-lysogenic strains of Escherichia coli in the presence of chloramphenicol to prevent prophage induction. The inhibitory effect of colicin E2 on transport systems was analyzed with cells of E. coli CP78(X). The dose of colicin E2 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 ['4C]methylthiogalactoside suggested that colicin E2 began to inhibit the influx rate of ,B-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 (8-galactoside transport and leakage of potassium ion by the colicin were extensive in cells lysogenic for wild X phage or Xind-, whereas the extent,s were slight in the nonlysogenic cells or cells carrying Xrex-prophage. It was concluded that the sensitization of membrane transport systems of E. coli cells to colicin E2 was achieved by the presence of the rex gene product of X phage.Colicin E2 is a protein antibiotic ofEscherichia coli with a molecular weight of 60,000. When sensitive E. coli cells adsorb the colicin, damage of cellular deoxyribonucleic acid (DNA) occurs at first, whereas other macromolecular syntheses continue for a relatively long time (18). Colicin E2 is similar in several points, such as receptor specificities, immunological reactions, and physical parameters, to colicin E3 (13), although the ultimate biochemical effects of these two colicins are quite different. Studies on the mode of action of colicin E3 have shown that the colicin has an intrinsic enzymatic activity to cleave 16S ribonucleic acid and cause the inactivation of the ribosome (4, 5, 21). Several attempts to find deoxyribonuclease activity associated with colicin E2 had been negative (1,18,22); however, recent studies by Saxe showed that purified colicin E2 preparations possess deoxyribonuclease activity to introduce one single-strand scission in supercoiled X phage DNA (24,25). Although this finding implies the nucleolytic activity of colicin E2 as the basis of the in vivo action, the isolation of a mutant in which the colicin stops cell division without DNA degradation indicates that the primary cause of killing by the colicin is not necessarily DNA damage (3). In the case of colicins like E, and K, rapid loss of potassium and other cations from the treated cells is observed, and it seems likely that the mode of action involves structural alteration of the cell membrane (10,17,18). However, it has been believed that colicin E2 has no such activity to induce loss of ...

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“…To determine which X genes are involved, the effect of several mutant prophages was tested. The results indicate that the reduction in solubilization is due to the product of the rex gene of the X prophage (Saxe, 1974). Endo et al (1963) reported that colicin E2 induces the development of X from its prophage.…”

Section: Resultsmentioning

confidence: 92%

“…The effects of E2 on a pair of isogenic bacterial strains, one nonlysogen and the other lysogenic for X ind-, were tested. The inhibition of DNA breakdown is evident only at the high E2 multiplicity and at late times (Saxe, 1974). To determine which X genes are involved, the effect of several mutant prophages was tested.…”

Section: Resultsmentioning

confidence: 99%

Action of colicin E2 on supercoiled λ DNA. I. Experiments in vivo

Ls¹

1975

Biochemistry

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A lambda DNA supercoil system has been developed to study the effects of colicin E2 on DNA in vivo. Colicin E2, a protein antibiotic synthesized by strains of coliform bacteria that carry the Col E2 plasmid, had as its most conspicious effect damage to the DNA of sensitive strains. Colicine E2 attacks the supercoiled molecul formed by labeled lambda DNA in superinfected cells as well as it attacks the bacterial DNA. The rate and extent of acid solubilization of the lambda supercoils and of host bacterial DNA induced by E2 treatment are nearly identical. Treatment of superinfected cells with colicin E2 results in the progressive conversion of lambda DNA supercoils to open circles and/or linear full lenght molecules, and subsequently to fragments less than full lambda in size. The first endonucleolytic reactions are single-strand and or double-strand breaks. The rate of supercoil breakdown as well as the final percent supercoils remaining unconverted, the size of the final lambda fragments, and the extent of solubilization are dependent on the multiplicity of colicin used. Additions of trypsin to E2-treated superinfected cells results in a cessation of further breakdown of the lambda molecules, presumably as a result of digestion of accessible colicin molecules. Energy is essential for an early event in colicin E2 action. The host enzymes, endonuclease I and Rec BC, may be instrumental in the nucleolytic process caused by colicin E2: endonuclease I in reaction preceding cell killing and Rec BC in a secondary degradation of the bacterial DNA.

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Reduction of colicin E2-induced DNA breakdown by the rex gene of λ prophage

Cited by 7 publications

References 13 publications

Colicinogeny and related phenomena.

Colicinogeny and related phenomena.

Inhibitory Effect of Colicin E ₂ on Transport Systems of Escherichia coli in the Presence of the rex Gene of λ Prophage

Action of colicin E2 on supercoiled λ DNA. I. Experiments in vivo

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Reduction of colicin E2-induced DNA breakdown by the rex gene of λ prophage

Cited by 7 publications

References 13 publications

Colicinogeny and related phenomena.

Colicinogeny and related phenomena.

Inhibitory Effect of Colicin E 2 on Transport Systems of Escherichia coli in the Presence of the rex Gene of λ Prophage

Action of colicin E2 on supercoiled λ DNA. I. Experiments in vivo

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Inhibitory Effect of Colicin E ₂ on Transport Systems of Escherichia coli in the Presence of the rex Gene of λ Prophage