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PMID: 9748461 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Regulation of Escherichia coli secA by cellular protein secretion proficiency requires an intact gene X signal sequence and an active translocon.

Journal of bacteriology ·Vol. 180 ·No. 19 ·1998-10-00 ·Pages 5240-2

Oliver D, Norman J, Sarker S

Abstract

secA is translationally regulated by the protein secretion proficiency state of the Escherichia coli cell. This regulation was explored by making signal sequence mutations in the gene upstream of secA, gene X, which promotes secA translational coupling. Gene X signal sequence mutants were constitutive for secA expression, while prlA alleles partially restored secA regulation. These results show that interaction of the pre-gene X protein with the translocon is required for proper secA regulation. Furthermore, gene X signal sequence mutations disrupted secA regulation only in the cis configuration. We propose that nascent pre-gene X protein interacts with the translocon during its secretion to constitute the secretion sensor.

MeSH Terms
Adenosine Triphosphatases/genetics Bacterial Proteins/genetics,metabolism Chromosomes, Bacterial/genetics Escherichia coli/genetics Escherichia coli Proteins Gene Expression Regulation, Bacterial/genetics Membrane Transport Proteins Mutation Plasmids/genetics Protein Sorting Signals/genetics SEC Translocation Channels SecA Proteins
Chemicals
Bacterial Proteins Escherichia coli Proteins Membrane Transport Proteins Protein Sorting Signals SEC Translocation Channels Adenosine Triphosphatases SecA Proteins
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Oliver D
Department of Molecular Biology and Biochemistry, Wesleyan University, Middletown, Connecticut 06459, USA doliver@wesleyan.edu
Norman J
Sarker S
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27 references, click to expand
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Article Info
Journal
Journal of bacteriology
Abbr.
J Bacteriol
ISSN
0021-9193
Published
1998-10-00
Pages
5240-2
Language
English
Region
United States
NLM ID
2985120R
PMCID
PMC107564
Subset
IM
Grants
NIGMS NIH HHS · R01 GM042033 · United States
NIGMS NIH HHS · GM42033 · United States
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