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PMID: 1406588 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Insertional disruption of the nusB (ssyB) gene leads to cold-sensitive growth of Escherichia coli and suppression of the secY24 mutation.

Molecular & general genetics : MGG ·Vol. 234 ·No. 3 ·1992-09-00 ·Pages 429-32

Taura T, Ueguchi C, Shiba K, Ito K

Abstract

The Escherichia coli gene ssyB was cloned and sequenced. The ssyB63 (Cs) mutation is an insertion mutation in nusB, while the nusB5 (Cs) mutation suppresses secY24, indicating that inactivation of nusB causes cold-sensitive cell growth as well as phenotypic suppression of secY24. The correct map position of nusB is 9.5 min rather than 11 min as previously assigned. It is located at the distal end of an operon that contains a gene showing significant homology with a Bacillus subtilis gene involved in riboflavin biosynthesis.

Related Genes

nusB secY ssyB

MeSH Terms

Amino Acid Sequence Bacterial Proteins/genetics Base Sequence Chromosome Mapping Cold Temperature DNA, Bacterial/genetics Escherichia coli/genetics,growth & development Escherichia coli Proteins Genes, Bacterial Genes, Suppressor Genetic Complementation Test Molecular Sequence Data Mutagenesis, Insertional Polymerase Chain Reaction Transcription Factors/genetics Transcription, Genetic

Chemicals

Bacterial Proteins DNA, Bacterial Escherichia coli Proteins NusB protein, E coli Transcription Factors

Authors & Affiliations

4 authors, click to expand affiliations / ORCID

Taura T

Institute for Virus Research, Kyoto University, Japan.

Ueguchi C

Shiba K

Ito K

References (24)

24 references, click to expand

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Article Info

Journal

Molecular & general genetics : MGG

Abbr.

Mol Gen Genet

ISSN

0026-8925

DOI

10.1007/BF00538702

Published

1992-09-00

Pages

429-32

Language

English

Region

Germany

NLM ID

0125036

Subset

Databases

GENBANK

X64395

External Links

PubMed source DOI: 10.1007/BF00538702

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Insertional disruption of the nusB (ssyB) gene leads to cold-sensitive growth of Escherichia coli and suppression of the secY24 mutation.

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