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PMID: 328928 Published · ppublish English Journal Article Research Support, U.S. Gov't, Non-P.H.S. Research Support, U.S. Gov't, P.H.S.

Membrane damage in abortive infections of colicin Ib-containing Escherichia coli by bacteriophage T5.

Journal of virology ·Vol. 23 ·No. 1 ·1977-07-00 ·Pages 98-105

Cheung AK, Duckworth DH

Abstract

Strains of Escherichia coli K-12 containing the colicin Ib (Col Ib) factor did not produce progeny phage when infected by T5 bacteriophage. The cells were killed but did not lyse. If sodium dodecyl sulfate (SDS) was added to T5-infected E. coli (Col Ib), lysis occurred prematurely, but no phage were produced. SDS had no effect on infected cells that did not contain the Col Ib factor or on uninfected cells with or without the Col Ib factor. Cells that contained a mutant Col Ib factor that allowed phage production were not prematurely lysed after infection in the presence of SDS. When the Col Ib-containing cells were infected, protein and RNA synthesis stopped at about 10 min postinfection, and the cells released abnormal amounts of 32P-containing material, ATP, and beta-galactosidase into the medium. They also became inhibited in their ability to accumulate thiomethyl-beta-D-galactopyranoside and to utilize glycerol. Two alternative hypotheses are presented to explain these results.

MeSH Terms
Adenosine Triphosphate/metabolism Bacteriolysis Colicins/biosynthesis Coliphages/growth & development,metabolism Escherichia coli/drug effects,metabolism Galactosidases/metabolism Glycerol/metabolism Methylgalactosides/metabolism Mutation Sodium Dodecyl Sulfate/pharmacology Virus Replication
Chemicals
Colicins Methylgalactosides Sodium Dodecyl Sulfate Adenosine Triphosphate Galactosidases Glycerol
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Cheung A K
Duckworth D H
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30 references, click to expand
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Article Info
Journal
Journal of virology
Abbr.
J Virol
ISSN
0022-538X
Published
1977-07-00
Pages
98-105
Language
English
Region
United States
NLM ID
0113724
PMCID
PMC515804
Subset
IM
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