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J Bacteriol. 1979 February; 137(2): 878-884
Copyright © 1979, American Society for Microbiology. All Rights Reserved.

Influence of the Lactose Plasmid on the Metabolism of Galactose by Streptococcus lactis

Donald J. LeBlanc, Vaughan L. Crow, Linda N. Lee and Claude F. Garon{dagger}

1 Laboratory of Microbiology and Immunology, National Institute of Dental Research, Bethesda, Maryland 20014

ABSTRACT

Streptococcus lactis strain DR1251 was capable of growth on lactose and galactose with generation times, at 30°C, of 42 and 52 min, respectively. Phosphoenolpyruvate-dependent phosphotransferase activity for lactose and galactose was induced during growth on either substrate. This activity had an apparent Km of 5 x 10–5 M for lactose and 2 x 10–2 M for galactose. ß-D-Phosphogalactoside galactohydrolase activity was synthesized constitutively by these cells. Strain DR1251 lost the ability to grow on lactose at a high frequency when incubated at 37°C with glucose as the growth substrate. Loss of ability to metabolize lactose was accompanied by the loss of a 32-megadalton plasmid, pDR1, and Lac– isolates did not revert to a Lac+ phenotype. Lac– strains were able to grow on galactose but with a longer generation time. Galactose-grown Lac– strains were deficient in ß-D-phosphogalactoside galactohydrolase activity and phosphoenolpyruvate phosphotransferase activity for both lactose and galactose. There was also a shift from a predominantly homolactic to a heterolactic fermentation and a fivefold increase in galactokinase activity, relative to the Lac+ parent strain grown on galactose. These results suggest that S. lactis strain DR1251 metabolizes galactose primarily via the tagatose-6-phosphate pathway, using a lactose phosphoenolpyruvate phosphotransferase activity to transport this substrate into the cell. Lac– derivatives of strain DR1251, deficient in the lactose phosphoenolpyruvate phosphotransferase activity, appeared to utilize galactose via the Leloir pathway.

FOOTNOTES

{dagger} Laboratory of Biology of Viruses, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20014.

J Bacteriol. 1979 February; 137(2): 878-884
Copyright © 1979, American Society for Microbiology. All Rights Reserved.



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