The rcsB gene, a positive regulator of colanic acid biosynthesis in Escherichia coli, is also an activator of ftsZ expression

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Published in:Journal of Bacteriology Vol. 174; no. 12; pp. 3964 - 3971
Main Authors: GERVAIS, F. G, PHEONIX, P, DRAPEAU, G. R
Format: Journal Article
Language:English
Published: Washington, DC American Society for Microbiology 01-06-1992
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Wild-type genes which, when overexpressed, are capable of restoring the growth deficiency of the division mutant ftsZ84 of Escherichia coli on L medium containing no added NaCl have been isolated. One of these genes is rcsB, a positive regulator of colanic acid biosynthesis. A direct relationship between rcsB expression and FtsZ activity was observed, suggesting that RcsB specifically increases transcription of ftsZ, thus accounting for the restoration of colony formation by ftsZ84 mutant cells. Analysis of the 5' upstream sequence of rcsB revealed, in addition to the sigma 54 promoter sequence previously reported, a presumptive sigma 70 promoter and LexA-binding site plus an upstream sequence that is found to be essential for the expression of rcsB on a plasmid. The absence of the sigma 54 factor does not have a negative effect on the transcription of rcsB. The RcsB protein is an activator of its own synthesis, particularly in the presence of NaCl. Evidence which suggests that RcsB can be phosphorylated by a presumably modified EnvZ or PhoM sensor protein leading to a suppression of the growth deficiency of ftsZ84 mutant cells and to an increase in colanic acid production was obtained. We also demonstrated that the level of colanic acid is reduced when the cells carry a multicopy rcsC plasmid, suggesting that the RcsC sensor has phosphatase activity.
Research which suggests that ResB can be phosphorylated by a presumably modified EnvZ or PhoM sensor protein leading to a suppression of the growth deficiency of ftsZ84 mutant cells and to an increase in colanic acid production is presented.
Author G R Drapeau
P Phoenix
F G Gervais
AuthorAffiliation Department of Microbiology, Université de Montréal, Québec, Canada
AuthorAffiliation_xml – name: Department of Microbiology, Université de Montréal, Québec, Canada
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  givenname: F. G
  surname: GERVAIS
  fullname: GERVAIS, F. G
  organization: Univ. Montréal, dep. microbiologie, Montréal PQ H3C 3J7, Canada
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  surname: PHEONIX
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  givenname: G. R
  surname: DRAPEAU
  fullname: DRAPEAU, G. R
  organization: Univ. Montréal, dep. microbiologie, Montréal PQ H3C 3J7, Canada
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Issue 12
Keywords Regulation(control)
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Escherichia coli
Cell division
Regulator gene
Bacteria
Activation
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SSID ssj0014452
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Wild-type genes which, when overexpressed, are capable of restoring the growth deficiency of the division mutant ftsZ84 of Escherichia coli on L medium...
Research which suggests that ResB can be phosphorylated by a presumably modified EnvZ or PhoM sensor protein leading to a suppression of the growth deficiency...
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StartPage 3964
SubjectTerms Amino Acid Sequence
Bacteria
Bacterial Proteins - chemistry
Bacterial Proteins - genetics
Bacteriology
Base Sequence
Biological and medical sciences
Cellular biology
Cytoskeletal Proteins
DNA-Binding Proteins
DNA-Directed RNA Polymerases
Escherichia coli - genetics
Escherichia coli - growth & development
Escherichia coli - metabolism
Escherichia coli Proteins
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation, Bacterial - genetics
Genetic Complementation Test
Genetics
Medical research
Microbiology
Molecular Sequence Data
Phosphorylation
Plasmids - genetics
Polysaccharides - biosynthesis
Polysaccharides, Bacterial - biosynthesis
Promoter Regions, Genetic
Proteins
Recombinant Fusion Proteins - genetics
RNA Polymerase Sigma 54
Serine Endopeptidases
Sigma Factor - genetics
Transcription Factors
Title The rcsB gene, a positive regulator of colanic acid biosynthesis in Escherichia coli, is also an activator of ftsZ expression
URI http://jb.asm.org/content/174/12/3964.abstract
https://www.ncbi.nlm.nih.gov/pubmed/1597415
https://www.proquest.com/docview/227052014
https://search.proquest.com/docview/72984335
https://pubmed.ncbi.nlm.nih.gov/PMC206105
Volume 174
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