Calmes R
Infect Immun. 1978 Mar;19(3):934-42. doi: 10.1128/iai.19.3.934-942.1978.
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.
在代表变形链球菌四个血清遗传组的五株致龋菌株(HS6、AHT、FA1、NCTC 10449和SL1)中研究了乳糖的转运和水解机制。除HS6菌株外,在所有测试菌株中,乳糖的转运和水解系统分别具有磷酸烯醇丙酮酸(PEP)依赖性乳糖(Lac)磷酸转移酶(PT)系统和磷酸-β-半乳糖苷酶(P-β-gal)的特征。去密码细胞转运不可代谢的β-半乳糖苷模型邻硝基苯基-β-D-吡喃半乳糖苷(ONPG)和硫代甲基-β-D-吡喃半乳糖苷(TMG)需要PEP和Mg(2+)。用2-磷酸甘油酸(2-PG)替代PEP也能刺激Lac PT系统。其他潜在的高能磷酸供体(三磷酸腺苷、二磷酸腺苷、一磷酸腺苷和三磷酸鸟苷)不能刺激Lac PT系统。氟化钠对以PEP为能量来源的去密码细胞中的PEP依赖性Lac PT系统没有影响;然而,当使用2-PG作为能量来源时,F(-)抑制ONPG磷酸化。对于必须内源性产生PEP的完整细胞,浓度≥10 mM的F(-)的存在完全抑制Lac PT系统,推测是通过抑制2-PG水解酶(EC 4.2.1.11;烯醇酶)。完整细胞和去密码细胞都积累了一种TMG的磷酸化衍生物,其色谱行为与TMG-磷酸盐相同。经碱性磷酸酶处理后,该衍生物的R(f)与TMG相同。以ONPG为底物未检测到β-半乳糖苷酶(β-gal)活性;仅当提供ONPG-6-磷酸盐作为底物时才发生水解。根据以下标准可知,HS6菌株显然通过主动转运型系统转运乳糖,其中积累的细胞内产物是游离二糖:(i)去密码细胞中ONPG的转运和水解不受PEP刺激;(ii)在没有PEP的情况下发生ONPG水解;(iii)ONPG-6-磷酸盐未被水解。这些数据表明,除HS6菌株外,在所有测试菌株中,乳糖转运由PEP依赖性Lac PT系统介导,导致乳糖-磷酸盐积累,该乳糖-磷酸盐由一种类似于N群链球菌和金黄色葡萄球菌的P-β-gal的酶水解;相反,HS6菌株分别通过PEP非依赖性转运系统和β-gal转运和水解乳糖。