Involvement of phosphoenolpyruvate in the catabolism of caries-conducive disaccharides by Streptococcus mutans: lactose transport.
The mechanisms for transport and hydrolysis of lactose were investigated in five cariogenic strains (HS6, AHT, FA1, NCTC 10449, and SL1) representing the four serogenetic groups of Streptococcus mutans. The systems for transport and hydrolysis of lactose had the characteristics of a phosphoenolpyruvate (PEP)-dependent lactose (Lac) phosphotransferase (PT) system and phospho-beta-galactosidase (P-beta-gal), respectively, in all strains tested, except strain HS6. Decryptified cells required PEP and Mg(2+) for transport of the non-metabolizable model beta-galactosides o-nitrophenyl-beta-d-galactopyranoside (ONPG) and thiomethyl-beta-d-galactopyranoside (TMG). Substitution of 2-phosphoglycerate (2-PG) for PEP also stimulated the Lac PT system. Other potential high-energy phosphate donors (adenosine tri-, di-, and monophosphates and guanosine triphosphate) did not stimulate the Lac PT system. Sodium fluoride had no effect upon the PEP-dependent Lac PT system in decryptified cells with PEP as the energy source; however, when 2-PG was used as the energy source, F(-) inhibited ONPG phosphorylation. With intact cells which must generate PEP endogenously, the presence of F(-) in concentration >/= 10 mM completely inhibited the Lac PT system, presumably through inhibition of 2-PG hydrolyase (EC 4.2.1.11; enolase). Both intact and decryptified cells accumulated a phosphorylated derivative of TMG that behaved chromatographically as TMG-phosphate. After alkaline phosphatase treatment, the derivative had an R(f) identical to that of TMG. No beta-galactosidase (beta-gal) activity was detected with ONPG as the substrate; hydrolysis occurred only when ONPG-6-phosphate was supplied as the substrate. Strain HS6 apparently transported lactose by an active transport-type system in which the accumulated intracellular product was the free disaccharide based on the following criteria: (i) ONPG transport and hydrolysis in decryptified cells was not stimulated by PEP; (ii) ONPG hydrolysis occurred in the absence of PEP; and (iii) ONPG-6-phosphate was not hydrolyzed. These data indicate that, in all strains tested except strain HS6, lactose transport was mediated by a PEP-dependent Lac PT system, resulting in accumulation of lactose-phosphate that was hydrolyzed by an enzyme similar to the P-beta-gal of group N streptococci and Staphylococcus aureus; conversely, strain HS6 transported and hydrolyzed lactose by a PEP-independent transport system and beta-gal, respectively.
D001692:Biological Transport; D003470:Culture Media; D004790:Enzyme Induction; D005459:Fluorides / Q000494:pharmacology; D005690:Galactose / Q000378:metabolism; D007785:Lactose / Q000378:metabolism*; D008756:Methylgalactosides / Q000378:metabolism; D009598:Nitrophenylgalactosides / Q000378:metabolism; D010728:Phosphoenolpyruvate / Q000378:metabolism*; D010731:Phosphoenolpyruvate Sugar Phosphotransferase System / Q000378:metabolism*; D010770:Phosphotransferases / Q000378:metabolism*; D013295:Streptococcus mutans / Q000235:genetics / Q000378:metabolism*
D003470:Culture Media; D008756:Methylgalactosides; D009598:Nitrophenylgalactosides; D010728:Phosphoenolpyruvate; D010770:Phosphotransferases; D010731:Phosphoenolpyruvate Sugar Phosphotransferase System; D007785:Lactose; D005459:Fluorides; D005690:Galactose
J Bacteriol. 1977 May;130(2):583-95
122509
Caries Res. 1977;11 Suppl 1:262-91
318573
J Bacteriol. 1976 May;126(2):751-7
770452
Infect Immun. 1977 Apr;16(1):318-27
873612
J Dent Res. 1975 Mar-Apr;54(2):330-8
1054344
J Dent Res. 1976 Apr;55 Spec No:C87-96
1063155
Annu Rev Med. 1975;26:121-36
1096752
Ciba Found Symp. 1975;(31):225-41
1097216
Nutr Rev. 1975 Dec;33(12):353-61
1105259
J Bacteriol. 1975 Dec;124(3):1475-81
1194241
Biochem Biophys Res Commun. 1974 Aug 5;59(3):879-86
4137900
Proc Natl Acad Sci U S A. 1967 Jul;58(1):274-9
4292101
J Bacteriol. 1972 May;110(2):604-15
4336691
J Bacteriol. 1974 Sep;119(3):830-9
4368487
Helv Odontol Acta. 1974 Oct;18(2):101-13
4418000
J Gen Microbiol. 1974 Aug;83(2):327-38
4427102
J Dent Res. 1973 Nov-Dec;52(6):1209-15
4519056
J Bacteriol. 1972 Feb;109(2):784-9
4621686
Infect Immun. 1972 Sep;6(3):422-4
4637614
J Bacteriol. 1973 Oct;116(1):192-202
4745413
J Biol Chem. 1968 Apr 25;243(8):1881-5
4869132
Odontol Revy. 1970;21(2):143-52
4992207
Arch Biochem Biophys. 1971 Sep;146(1):167-74
5144023
Arch Oral Biol. 1968 Jun;13(6):609-17
5244285
Arch Oral Biol. 1968 Jul;13(7):827-30
5244304
Helv Odontol Acta. 1966 Oct;10(2):101-13
5334243
J Bacteriol. 1970 Jun;102(3):804-9
5429725
J Bacteriol. 1970 Nov;104(2):808-13
5489437
J Bacteriol. 1968 Jun;95(6):2270-4
5669899
J Bacteriol. 1969 Aug;99(2):603-10
5808082
Biochim Biophys Acta. 1966 Jan 4;112(1):63-73
5947899
J Nutr. 1967 Sep;93(1):65-76
6053761
Proc Natl Acad Sci U S A. 1964 Oct;52:1067-74
14224387
J Dent Res. 1960 Jan-Feb;39:116-23
14407868
J Bacteriol. 1950 Oct;60(4):381-92
14784466
J Biol Chem. 1951 Nov;193(1):265-75
14907713
Infect Immun. 1974 Nov;10(5):1170-9
16558106