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PMID: 6352679 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Novel mechanism of cell division inhibition associated with the SOS response in Escherichia coli.

Journal of bacteriology ·Vol. 156 ·No. 1 ·1983-10-00 ·Pages 243-50

D'Ari R, Huisman O

Abstract

Certain Escherichia coli strains were shown to possess a novel system of cell division inhibition, called the SfiC+ phenotype. SfiC+ filamentation had a number of properties similar to those of sfiA-dependent division inhibition previously described: (i) both are associated with the SOS response induced by expression of the recA(Tif) mutation, (ii) both are associated with cell death, (iii) both are amplified in mutants lacking the Lon protease, and (iv) both are suppressed by sfiB mutations. SfiC+ filamentation and sfiA-dependent division inhibition differed in (i) the physiological conditions under which loss of viability is observed, (ii) the extent of amplification in lon mutants, (iii) their genetic regulation (SfiC+ filamentation is not under direct negative control of the LexA repressor), and (iv) their genetic determinants (SfiC+ filamentation depends on a locus, sfiC+, near 28 min on the E. coli map and distinct from sfiA).

MeSH Terms
ATP-Dependent Proteases Cell Division DNA Replication Endopeptidases/physiology Escherichia coli/cytology,genetics Escherichia coli Proteins Genes, Bacterial Heat-Shock Proteins Mutation Protease La Rec A Recombinases/genetics,physiology Serine Endopeptidases Temperature
Chemicals
Escherichia coli Proteins Heat-Shock Proteins Rec A Recombinases Endopeptidases ATP-Dependent Proteases Serine Endopeptidases Lon protein, E coli Protease La
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
D'Ari R
Huisman O
References (33)
33 references, click to expand
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Article Info
Journal
Journal of bacteriology
Abbr.
J Bacteriol
ISSN
0021-9193
DOI
10.1128/jb.156.1.243-250.1983
Published
1983-10-00
Pages
243-50
Language
English
Region
United States
NLM ID
2985120R
PMCID
PMC215076
Subset
IM
External Links
PubMed source DOI: 10.1128/jb.156.1.243-250.1983 PMC Full Text View journal details
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