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PMID: 3117771 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Temporal control of colicin E1 induction.

Journal of bacteriology ·Vol. 169 ·No. 11 ·1987-11-00 ·Pages 5028-34

Salles B, Weisemann JM, Weinstock GM

Abstract

The expression of the gene encoding colicin E1, cea, was studied in Escherichia coli by using cea-lacZ gene fusions. Expression of the fusions showed the same characteristics as those of the wild-type cea gene: induction by treatments that damage DNA and regulation by the SOS response, sensitivity to catabolite repression, and a low basal level of expression, despite the presence of the fusion in a multicopy plasmid. Induction of expression by DNA-damaging treatments was found to differ from other genes involved in the SOS response (exemplified by recA), in that higher levels of DNA damage were required and expression occurred only after a pronounced delay. The delay in expression following an inducing treatment was more pronounced under conditions of catabolite repression, indicating that the cyclic AMP-cyclic AMP receptor protein complex may play a role in induction. These observations also suggest a biological rationale for the control of cea expression by the SOS response and the cyclic AMP-cyclic AMP receptor protein catabolite repression system.

MeSH Terms
Cloning, Molecular Colicins/biosynthesis,genetics Escherichia coli/genetics,metabolism,radiation effects Gene Expression Regulation Genes Genes, Bacterial Genes, Regulator Genotype Kinetics Plasmids Time Factors Transcriptional Activation Ultraviolet Rays beta-Galactosidase/genetics
Chemicals
Colicins beta-Galactosidase
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Salles B
Department of Biochemistry and Molecular Biology, University of Texas Medical School, Houston 77057.
Weisemann J M
Weinstock G M
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Article Info
Journal
Journal of bacteriology
Abbr.
J Bacteriol
ISSN
0021-9193
DOI
10.1128/jb.169.11.5028-5034.1987
Published
1987-11-00
Pages
5028-34
Language
English
Region
United States
NLM ID
2985120R
PMCID
PMC213904
Subset
IM
Grants
NIGMS NIH HHS · GM35247 · United States
NCI NIH HHS · N01-CO-23909 · United States
External Links
PubMed source DOI: 10.1128/jb.169.11.5028-5034.1987 PMC Full Text View journal details
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