Abstract
SecA is a dynamic protein that undergoes ATP-dependent membrane cycling to drive protein translocation across the Escherichia coli inner membrane. To understand more about this process, azide-resistant (azi) and signal sequence suppressor (prlD) alleles of secA were studied. We found that azide resistance is cold sensitive because of a direct effect on protein export, suggesting that SecA-membrane interaction is regulated by an endothermic step that is azide inhibitable. secG function is required for expression of azide-resistant and signal sequence suppressor activities of azi and prlD alleles, and in turn, these alleles suppress cold-sensitive and export-defective phenotypes of a secG null mutant. These remarkable genetic observations support biochemical data indicating that SecG promotes SecA membrane cycling and that this process is dependent on an endothermic change in SecA conformation.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adenosine Triphosphatases / chemistry
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Adenosine Triphosphatases / genetics*
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Adenosine Triphosphatases / metabolism
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Alleles
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Azides / pharmacology
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Bacterial Proteins / chemistry
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Bacterial Proteins / genetics*
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Bacterial Proteins / metabolism
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Biological Transport, Active / genetics
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Cold Temperature
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Drug Resistance, Microbial / genetics
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Escherichia coli / drug effects
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Escherichia coli / genetics*
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Escherichia coli / metabolism
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Escherichia coli Proteins*
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Gene Deletion
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Genes, Bacterial
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Membrane Proteins / genetics*
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Membrane Proteins / metabolism
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Membrane Transport Proteins*
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Mutation
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Phenotype
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Protein Conformation
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Protein Sorting Signals / genetics
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SEC Translocation Channels
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SecA Proteins
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Suppression, Genetic
Substances
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Azides
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Bacterial Proteins
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Escherichia coli Proteins
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Membrane Proteins
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Membrane Transport Proteins
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Protein Sorting Signals
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SEC Translocation Channels
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SecG protein, E coli
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Adenosine Triphosphatases
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SecA Proteins