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

J. Stock, A. Borczuk, F. Chiou, J. E.B. Burchenal

Research output: Contribution to journalArticle

26 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)8364-8368
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume82
Issue number24
DOIs
StatePublished - 1985

All Science Journal Classification (ASJC) codes

  • General

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