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Gene Review

galE  -  UDP-galactose-4-epimerase

Salmonella enterica subsp. enterica serovar Typhimurium str. LT2

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Disease relevance of galE

  • Stable restriction-deficient, modification-proficient galE (JR501) and F'galE+ (JR502) strains of Salmonella typhimurium were constructed and the effects of restriction on transformation by plasmid pBR322 were tested [1].
  • Growth on galactose-supplemented medium restored the smooth phenotype, as indicated by phage sensitivity to three of the four galE strains, but only partially so for the strain 117 galE mutant [2].
  • Brucella melitensis 16M: characterisation of the galE gene and mouse immunisation studies with a galE deficient mutant [3].
  • The galE gene of Streptomyces lividans was used to probe a cosmid library harbouring Brucella melitensis 16M DNA and the nucleotide sequence of a 2.5 kb ClaI fragment which hybridised was determined [3].

High impact information on galE

  • In addition, undecaprenol-linked O antigen was detectable at the periplasmic face of the inner membrane within 30 sec after addition of galactose to a galE deep rough double mutant, and it accumulated stably in that location [4].
  • Salmonella typhimurium galE mutants in which O-antigen synthesis is dependent on addition of exogenous galactose were employed, and the distribution and fate of pulse-synthesized O antigen was examined by indirect ferritin labeling with anti-O-antigen IgG of spheroplasts prepared by treatment with lysozyme/EDTA [4].
  • The galE derivative of strain 381 comprised two components: galactose sensitive, thought to be the original mutant; and galactose resistant, presumably by a second mutation reducing galK or galT function or both [2].
  • The galE mutant of strain 110 was somewhat sensitive to galactose, as shown by retardation of growth; its 50% lethal dose, ca. 500 CFU, was not much greater than the ca. 200 CFU value for its parent [2].
  • galE mutants were isolated from three mouse-virulent strains of Salmonella choleraesuis (of group C1, O antigen 6,7) by selection for resistance to 2-deoxygalactose [2].

Biological context of galE

  • When normal lipopolysaccharide synthesis is restored either genetically or by furnishing exogenous galactose (galE point mutants that can still use it), the cells are not longer competent for transfection [5].
  • The galE gene on the B. melitensis 16M chromosome was disrupted by insertional inactivation and these mutants lacked UDP-galactose-4-epimerase activity but no discernible differences in LPS structure between parent and the mutants were observed [3].
  • One B. melitensis 16M galE mutant, Bm92, was assessed for virulence in CD-1 and BALB/c mice and displayed similar kinetics of invasion and persistence in tissues compared with the parent bacterial strain [3].

Associations of galE with chemical compounds

  • The most amenable strains are blocked by defects in the addition of galactose units I and II of the lipopolysaccharide by the inability to synthesize uridine 5'-diphosphate-galactose (galE point mutants and gal deletion mutants) [5].
  • Aromatic (aroA), galactose epimerase (galE), and diaminopimelic acid (dap) mutants of strain 3860C all resulted in much less fluid response, mucosal invasion, and mucosal damage compared with those by the parent organism [6].

Other interactions of galE

  • Only those mutants with an Rc or Rd2 chemotype, due to galE or rfaF mutations, respectively, gave efficiencies greater than 10(5) transformants per microgram of DNA, frequencies 8- to 630-fold higher than with smooth strains or other rough mutants [7].
  • DNA sequences flanking the B. melitensis galE gene shared no identity with other gal genes and, as for B. abortus, were located adjacent to a mazG homologue [3].


  1. Transformation in restriction-deficient Salmonella typhimurium LT2. Tsai, S.P., Hartin, R.J., Ryu, J. J. Gen. Microbiol. (1989) [Pubmed]
  2. Some galE mutants of Salmonella choleraesuis retain virulence. Nnalue, N.A., Stocker, B.A. Infect. Immun. (1986) [Pubmed]
  3. Brucella melitensis 16M: characterisation of the galE gene and mouse immunisation studies with a galE deficient mutant. Petrovska, L., Hewinson, R.G., Dougan, G., Maskell, D.J., Woodward, M.J. Vet. Microbiol. (1999) [Pubmed]
  4. An intermediate step in translocation of lipopolysaccharide to the outer membrane of Salmonella typhimurium. Mulford, C.A., Osborn, M.J. Proc. Natl. Acad. Sci. U.S.A. (1983) [Pubmed]
  5. Transfectability of rough strains of Salmonella typhimurium. Bursztyn, H., Sgaramella, V., Ciferri, O., Lederberg, J. J. Bacteriol. (1975) [Pubmed]
  6. Virulence of wild and mutant strains of Salmonella typhimurium in ligated intestinal segments of calves, pigs, and rabbits. Clarke, R.C., Gyles, C.L. Am. J. Vet. Res. (1987) [Pubmed]
  7. Transformation of Salmonella typhimurium with plasmid DNA: differences between rough and smooth strains. MacLachlan, P.R., Sanderson, K.E. J. Bacteriol. (1985) [Pubmed]
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