Compensatory Mutations in Receptor Function: A Reevaluation of the Role of Methylation in Bacterial Chemotaxis

During bacterial chemotaxis membrane receptor proteins are methylated and demethylated at glutamate residues. The generally accepted view is that these reactions play an essential role in the chemosensing mechanism. Strains may be isolated, however, that exhibit chemotaxis in the complete absence of...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 1985-12, Vol.82 (24), p.8364-8368
Main Authors: Stock, Jeff, Borczuk, Alain, Chiou, Faye, Burchenal, J. E. B.
Format: Article
Language:English
Subjects:
Bacterial Proteins - genetics
Bacteriology
Biochemistry
Biological and medical sciences
Cells
Chemotaxis
Chromosome Mapping
Enzymes
Escherichia coli - genetics
Escherichia coli - physiology
Esterases - genetics
Fundamental and applied biological sciences. Psychology
Genetic mutation
Glutamine - metabolism
Membrane Proteins - genetics
Methyl-Accepting Chemotaxis Proteins
Methylation
Methyltransferases - genetics
Microbiology
Motility, taxis
Movement
Operons
Rates of change
Receptors
Suppression, Genetic
Swimming
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Summary:During bacterial chemotaxis membrane receptor proteins are methylated and demethylated at glutamate residues. The generally accepted view is that these reactions play an essential role in the chemosensing mechanism. Strains may be isolated, however, that exhibit chemotaxis in the complete absence of methylation. These are readily obtained by selecting for chemotactic variants of a mutant that completely lacks the methylating enzyme. Methyltransferase activity is not restored; instead, the sensory-motor apparatus is genetically restructured to compensate for the methylation defect. Genetic and biochemical analyses show that the compensatory mutational locus is the structural gene for the demethylating enzyme. Thus, although mutants lacking either the methylating or demethylating enzymes are nonchemotactic, strains defective in both activities exhibit almost-wild-type chemotactic ability.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.82.24.8364