Transposon-insertion mutants of Escherichia coli K12 defective in a component common to galactose and ribose chemotaxis

Mol Gen Genet. 1979 Mar 20;171(2):193-203. doi: 10.1007/BF00270005.


From a collection of 8,000 transposon-insertion mutants of Escherichia coli K12 we identified two mutations, trg-1::Tn5 and trg-2::Tn10, that simultaneously eliminate chemotactic response to ribose and galactose, two attractants recognized by independent receptors. We show that these transposon-insertions confer a Trg phenotype, indicating that this specific pattern of tactic defects is a null phenotype. The two mutation sites are cotransductionally linked to an extend consistent with placement in the same gene. The Trg phenotype of a family of deletion mutants produced by curing trg-2::Tn10 implies that trg is a single gene. Experiments with appropriate F-primes and Hfr's locate the trg locus at approximately 31 min on the linkage map, with a marker order: pyrF-rac-(P.O. 43)-trg-man. We also found one trg mutant whose Trg phenotype was not linked to a transposon-insertion but is probably the result of a mutator activity in the parent strain. Selection of transposon-insertions near, but not in trg allowed demonstration of a very close linkage between the spontaneous trg-3 and the transposon-generated trg's, indicating all three mutations are probably in the same gene. In our manipulations of transposon-insertions we found that Tn5 had a tendency to translocate from its initial site of insertion while Tn10 was relatively stable. The trg-product is probably a chemotactic signal transducer, which interacts directly with two independent receptor proteins and transmits information to the central chemotactic machinery.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Chemotaxis*
  • Chromosome Mapping
  • Chromosomes, Bacterial
  • Escherichia coli / drug effects
  • Escherichia coli / genetics*
  • Galactose / pharmacology*
  • Genes
  • Mutation*
  • Phenotype
  • Receptors, Drug / genetics
  • Recombination, Genetic*
  • Ribose / pharmacology*
  • Transduction, Genetic


  • Receptors, Drug
  • Ribose
  • Galactose