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PMID: 3098730 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Genetic and morphological characterization of ftsB and nrdB mutants of Escherichia coli.

Journal of bacteriology ·Vol. 169 ·No. 1 ·1987-01-00 ·Pages 19-25

Taschner PE, Verest JG, Woldringh CL

Abstract

The ftsB gene of Escherichia coli is believed to be involved in cell division. In this report, we show that plasmids containing the nrdB gene could complement the ftsB mutation, suggesting that ftsB is an allele of nrdB. We compared changes in the cell shape of isogenic nrdA, nrdB, ftsB, and pbpB strains at permissive and restrictive temperatures. Although in rich medium all strains produced filaments at the restrictive temperature, in minimal medium only a 50 to 100% increase in mean cell mass occurred in the nrdA, nrdB, and ftsB strains. The typical pbpB cell division mutant also formed long filaments at low growth rates. Visualization of nucleoid structure by fluorescence microscopy demonstrated that nucleoid segregation was affected by nrdA, nrdB, and ftsB mutations at the restrictive temperature. Measurements of beta-galactosidase activity in lambda p(sfiA::lac) lysogenic nrdA, nrdB, and ftsB mutants in rich medium at the restrictive temperature showed that filamentation in the nrdA mutant was caused by sfiA (sulA) induction, while filamentation in nrdB and ftsB mutants was sfiA independent, suggesting an SOS-independent inhibition of cell division.

MeSH Terms
Alleles Cell Division Escherichia coli/genetics Genes, Bacterial Microscopy, Fluorescence Mutation Plasmids Temperature beta-Galactosidase/genetics,metabolism
Chemicals
beta-Galactosidase
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Taschner P E
Verest J G
Woldringh C L
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32 references, click to expand
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Article Info
Journal
Journal of bacteriology
Abbr.
J Bacteriol
ISSN
0021-9193
DOI
10.1128/jb.169.1.19-25.1987
Published
1987-01-00
Pages
19-25
Language
English
Region
United States
NLM ID
2985120R
PMCID
PMC211728
Subset
IM
External Links
PubMed source DOI: 10.1128/jb.169.1.19-25.1987 PMC Full Text View journal details
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