Bacterial chemotaxis in the absence of receptor carboxylmethylation.
Although chemoreceptor methylation in Salmonella typhimurium and Escherichia coli has been shown to be at the core of the chemotactic phenomenon, mutants in the gene (cheR) that codes for the methylating enzyme still respond and adapt to repellent stimuli. Analyses of receptor methylation and transferase activity show that this behavior is not due to residual transferase activity. That receptor methylation is not absolutely required for chemotactic sensory processing is confirmed by the isolation of cheR pseudorevertants that remain defective in receptor methylation, yet are able to respond to gradients on semi-solid tryptone agar. A detailed comparison of cheR and wild-type responses indicates that chemotaxis is mediated by at least two interdependent adaptation systems, only one of which involves receptor methylation. The interaction of these two systems produces the full response in wild-type cells. Methylation-deficient mutants exhibit a partial response and retain some chemotactic ability.
D000255:Adenosine Triphosphate / Q000502:physiology; D001426:Bacterial Proteins; D002628:Chemoreceptor Cells / Q000502:physiology; D002633:Chemotaxis; D004926:Escherichia coli / Q000201:enzymology / Q000502:physiology*; D008715:Methionine / Q000502:physiology; D008780:Methyltransferases / Q000378:metabolism; D009154:Mutation
D001426:Bacterial Proteins; D000255:Adenosine Triphosphate; D008715:Methionine; D008780:Methyltransferases