Compensatory mutations in receptor function: a reevaluation of the role of methylation in bacterial chemotaxis.

摘要: 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, exhibit complete absence of methylation. These readily obtained by selecting for chemotactic variants a mutant completely lacks methylating enzyme. Methyltransferase activity not restored; instead, sensory-motor apparatus genetically restructured to compensate methylation defect. Genetic biochemical analyses show compensatory mutational locus structural gene demethylating Thus, although mutants lacking either or enzymes nonchemotactic, strains defective both activities almost-wild-type ability.