Alteration of the Escherichia coli membrane by addition of bacteriophage T4 protein synthesized after infection

Ennis, Herbert L.; Kievitt, K D

doi:10.1128/jvi.22.2.553-560.1977

Cited by 5 publications

(4 citation statements)

References 32 publications

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“…Group 3 resembles the smaller T-phages of Escherichia coli (25). It is known that certain phages of E. coli cause the insertion of new proteins into the plasma t Present address: Laboratory of Microbial Structure and Function, National Institute of Allergy and Infectious Disease, Rocky Mountain Laboratory, Hamilton, MT 59840. membrane (8,39) and also affect membrane lipid synthesis (28). The latter phenomenon is particularly significant for amber mutants of the filamentous coliphage fl(M13) (28).…”

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confidence: 99%

Membrane composition and virus susceptibility of Acholeplasma laidlawii

Steinick¹,

Wieslander²,

Johansson³

et al. 1980

J Bacteriol

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The membrane composition of 11 strains ofAcholeplasma laidlawii, including three strains persistently infected with mycoplasmaviruses MVL51, MVL2, and MVL3, was studied and correlated with mycoplasmavirus sensitivity. Membranes of the strains had similar sodium dodecyl sulfate-polyacrylamide gel electrophoresis patterns, and all strains were inhibited by an antiserum produced against membranes from one of the strains. The amounts of integral membrane proteins solubilized by the nonionic detergent Tween 20 differed considerably. Therefore, characteristic crossed immunoelectrophoresis patterns were obtained for each strain. Strains persistently infected with MVL2 and MVL3 were notably different from the noninfected host. The ability to propagate any of the viruses was not correlated with sodium dodecyl sulfate-polyacrylamide gel electrophoresis or crossed immunoelectrophoresis patterns. The persistently infected strains had a characteristic lipid composition. MVL51-resistant strains, including a resistant clone selected from a sensitive strain, were characterized by a large monoglucosyldiglyceride/diglucosyldiglyceride ratio and trace amounts of diphosphatidylglycerol (as opposed to the sensitive strains). Differences in lipid composition in A. laidlawii seem to affect the relationship between cells and viruses.

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confidence: 99%

Membrane composition and virus susceptibility of Acholeplasma laidlawii

Steinick¹,

Wieslander²,

Johansson³

et al. 1980

J Bacteriol

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“…Two studies on the modification of host cell membranes by phage-induced proteins published since our work was done also described a quantitative association of gp46 with the host cell membranes and spheroplast envelopes (16,55). gp47 was not identified in either of these studies.…”

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confidence: 84%

“…By this criterion, although we found that gp47 was membrane associated, it also is not an integral membrane protein since incubation with NaClO4 released it from membranes. However, solubilization of a protein by chaotropic agents does not rule out the possibility that the protein has a functional interaction with the membrane (10,16,34,45), but it does show that the binding interaction is probably ionic.…”

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confidence: 99%

Membrane-associated DNase activity controlled by genes 46 and 47 of bacteriophage T4D and elevated DNase activity associated with the T4 das mutation

Mickelson¹,

Wiberg²

1981

J Virol

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Lethal, amber mutations in T4 genes 46 and 47 cause incomplete degradation of host DNA, premature arrest of phage DNA synthesis, accumulation of abnormal DNA replication intermediates, and defective recombination. These phenotypes can be explained by the hypothesis that genes 46 and 47 control a DNA exonuclease, but in vitro demonstration of such a nuclease has not yet been reported. Membrane and supematant fractions from 46-and 47-mutant-infected and 46+ 47+ control-infected cells were assayed for the presence of the protein products of these genes (i.e., gp46 and gp47) and for the ability to degrade various DNA substrates to acid-soluble products in vitro. The two proteins were found only on membranes. The membrane fraction from 46-47-mutant-infected cells digested native or heavily nicked Escherichia coli DNA to acid-soluble products three to four times slower than the membrane fraction from control-infected cells. No such effect was found in the cytoplasmic fractions. The effect on nuclease activity in membranes was the same whether 46-and 47-mutations were present singly or together. NaC104, a chaotropic agent, released both gp46 and gp47 from 46+ 47+ membranes, as well as the DNase activity controlled by genes 46 and 47. DNA cellulose chromatography of proteins released from membranes by NaCl04 showed that gp46 and gp47 bound to the native DNAs of both E. coli and T4. Thus, the overall enrichment of gp46 and gp47 relative to total T4 protein was 600-fold (10-fold in membranes, 2-fold more upon release from membranes by NaClO4, and 30-fold more upon elution from DNA cellulose). T4 das mutations, which partially suppress the defective phenotype of 46-and 47-mutants, caused a considerable increase in in vitro DNase activity in both membrane and cytoplasmic fractions. We obtained evidence that the das+ gene does not function to inhibit E. coli exonuclease I or V, endonuclease I, or the UV endonuclease of gene uvrA or to decrease the activity of T4 exonuclease A or the T4 gene 43 exonuclease.

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“…infection. Altematively, the late function may increase membrane fragility directly by modifying the membrane; changes in membrane composition after infection have been reported (11,12,15,21,34,46,51). Furrow and Pizer (15) have found that after T4 infection the relative rates of 32p; incorporation into phosphatidylglycerol and phosphatidylethanolamine were altered.…”

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confidence: 99%

Late effect of bacteriophage T4D on the permeability barrier of Escherichia coli

Thompson¹,

Wiberg²

1978

J Virol

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Cold centrifugation of lysis-inhibited Escherichia coli B infected with wildtype T4D results in extensive lysis beginning around 20 min after infection at 370C. Infection with an e mutant, which fails to make lysozyme, prevents lysis, but does not prevent a marked loss of K+ and Mg3+. The t gene product, thought to disrupt the cytoplasmic membrane in natural lysis, is not required for this handling-induced cation loss or lysis. Three lines of evidence argue that late protein synthesis is required to develop this potential for cation loss; the potential does not develop in infections by: (i) mutants defective in DNA synthesis, (ii) mutants defective in gene 55, and (iii) wild-type T4 when chloramphenicol is added at 6 min after infection. All late mutants examined, which are blocked in the major pathways of morphogenesis, do not prevent development of the potential. The evidence argues for a new, late effect of T4 infection on the cytoplasmic membrane.

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Alteration of the Escherichia coli membrane by addition of bacteriophage T4 protein synthesized after infection

Cited by 5 publications

References 32 publications

Membrane composition and virus susceptibility of Acholeplasma laidlawii

Membrane composition and virus susceptibility of Acholeplasma laidlawii

Membrane-associated DNase activity controlled by genes 46 and 47 of bacteriophage T4D and elevated DNase activity associated with the T4 das mutation

Late effect of bacteriophage T4D on the permeability barrier of Escherichia coli

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