Regulation of beta-galactoside phosphate accumulation in Streptococcus pyogenes by an expulsion mechanism.

Regulation of beta-galactoside phosphate accumulation in Streptococcus pyogenes by an expulsion mechanism.
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通过排出机制调节化脓性链球菌中β-半乳糖苷磷酸盐的积累。

DOI:
10.1073/pnas.77.9.5497
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发表时间:
1980
影响因子:
11.1
通讯作者:
Panos,C
Panos,C
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Reizer,J;Panos,C

文献摘要

被引文献

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在乳糖上预先生长的化脓性链球菌通过依赖磷酸烯醇丙酮酸的磷酸转移酶系统吸收葡萄糖、乳糖或甲基-d -硫代半乳糖苷(MeSGal或TMG)。MeSGalP在细胞中以MeSGalP的形式积累。在MeSGalP预载细胞中加入不同的糖后,发现了三个效应:(i)在加入果糖、蔗糖、邻硝基苯- β -d -半乳糖、甘油、6-脱氧葡萄糖、α -甲基d -葡糖苷、2-脱氧半乳糖、1-磷酸葡萄糖或6-磷酸葡萄糖后,细胞内MeSGalP浓度没有下降;(ii)乳糖、2-脱氧-d -葡萄糖或未标记的MeSGal引起的预先积累的MeSGalP的缓慢损失;(iii)葡萄糖或甘露糖引起细胞内MeSGalP的极快排出和葡萄糖胺引起的较慢排出后的短暂滞后。排出的化合物是游离的MeSGal,表明脱磷酸化参与了排出机制。脱氧葡萄糖抑制甘露糖引起的排出,氟或砷酸盐预中毒细胞阻止葡萄糖依赖性排出。这种排出是由于一种排出机制的激活,而不是由于MeSGalP的转换和内部MeSGal的泄漏,同时抑制MeSGal的内流。结果表明,需要磷酸化转移酶依赖的优先糖的易位或糖分解代谢物的积累才能进行驱逐激活。提出了碳水化合物利用过程中酶的合成调控与排出机制的意义。
Streptococcus pyogenes pregrown on lactose took up glucose, lactose, or methyl beta-D-thiogalactopyranoside (MeSGal or TMG) by a phosphoenolpyruvate-dependent phosphotransferase system. MeSGal accumulated in the cell as MeSGal-phosphate (MeSGalP). Three effects were noted when various sugars were added to MeSGal preloaded cells: (i) no decrease in intracellular MeSGalP concentration after addition of fructose, sucrose, o-nitrophenyl-beta-D-galactoside, glycerol, 6-deoxyglucose, alpha-methyl D-glucoside, 2-deoxygalactose, glucose 1-phosphate, or glucose 6-phosphate; (ii) slow loss of preaccumulated MeSGalP evoked by lactose, 2-deoxy-D-glucose, or unlabeled MeSGal; and (iii) a short lag followed by extremely rapid expulsion of intracellular MeSGalP elicited by glucose or mannose and a slower expulsion elicited by glucosamine. The expelled compound was free MeSGal, indicating the involvement of dephosphorylation in the expulsion mechanism. Deoxyglucose inhibited the expulsion evoked by mannose, and prepoisoning of cells with fluoride or arsenate prevented the glucose-dependent expulsion. The expulsion is due to activation of an expulsion mechanism rather than to turnover of MeSGalP and leak of internal MeSGal with concomitant inhibition of MeSGal influx. The results suggest the need for phosphotransferase-dependent translocation of a preferential sugar or accumulation of the sugar catabolite for expulsion activation. The significance of the expulsion mechanism in synthesis regulation of enzymes involved in carbohydrate utilization is proposed.