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

• 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
• ISSN: 0027-8424; 1091-6490
• DOI: 10.1073/pnas.82.24.8364

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.