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首页> 外文期刊>Journal of bacteriology >Genes Involved in Control of Galactose Uptake inLactobacillus brevis and Reconstitution of the Regulatory System in Bacillus subtilis
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Genes Involved in Control of Galactose Uptake inLactobacillus brevis and Reconstitution of the Regulatory System in Bacillus subtilis

机译：涉及控制短乳糖乳杆菌半乳糖摄取和枯草芽孢杆菌调节系统的重建的基因

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The heterofermentative lactic acid bacterium Lactobacillus brevis transports galactose and the nonmetabolizable galactose analogue thiomethyl-β-galactoside (TMG) by a permease-catalyzed sugar:H+ symport mechanism. Addition of glucose to L. brevis cells loaded with [14C]TMG promotes efflux and prevents accumulation of the galactoside, probably by converting the proton symporter into a uniporter. Such a process manifests itself physiologically in phenomena termed inducer expulsion and exclusion. Previous evidence suggested a direct allosteric mechanism whereby the phosphocarrier protein, HPr, phosphorylated at serine-46 [HPr(Ser-P)], binds to the galactose:H+ symporter to uncouple sugar transport from proton symport. To elucidate the molecular mechanism of inducer control in L. brevis, we have cloned the genes encoding the HPr(Ser) kinase, HPr, enzyme I, and the galactose:H+ symporter. The sequences of these genes were determined, and the relevant phylogenetic trees are presented. Mutant HPr derivatives in which the regulatory serine was changed to either alanine or aspartate were constructed. The clonedgalP gene was integrated into the chromosome ofBacillus subtilis, and synthesis of the mutant HPr proteins in this organism was shown to promote regulation of GalP, as expected for a direct allosteric mechanism. We have thus reconstituted inducer control in an organism that does not otherwise exhibit this phenomenon. These results are consistent with the conclusion that inducer exclusion and expulsion in L. brevis operates via a multicomponent signal transduction mechanism wherein the presence of glycolytic intermediates such as fructose 1,6-bisphosphate (the intracellular effector), derived from exogenous glucose (the extracellular effector), activates HPr(Ser) kinase (the sensor) to phosphorylate HPr on Ser-46 (the messenger), which binds to the galactose:H+ symporter (the target), resulting in uncoupling of sugar transport from proton symport (the response). This cascade allows bacteria to quickly respond to changes in external sugar concentrations. Understanding the molecular mechanism of inducer control advances our knowledge of the link between metabolic and transport processes in bacteria.
机译：短发酵乳酸菌 Levitobacillus brevis 通过渗透酶催化的糖：H + 转运机制转运半乳糖和不可代谢的半乳糖类似物硫代甲基-β-半乳糖苷（TMG）。在 L中添加葡萄糖。装有[ 14 C] TMG的灯盏花细胞可促进外流并防止半乳糖苷的积累，这可能是通过将质子同向体转化为单向体而实现的。这种过程在生理上表现为被称为诱导者驱逐和排斥的现象。先前的证据表明存在直接的变构机制，即磷酸丝氨酸46 [HPr（Ser-P）]磷酸化的磷酸载体蛋白HPr与半乳糖：H + 转运蛋白结合，使糖转运与质子转运体解耦。为了阐明 L中诱导子控制的分子机制。 brevis ，我们已经克隆了编码HPr（Ser）激酶，HPr，酶I和半乳糖：H + 同向转运体的基因。确定了这些基因的序列，并提出了相关的系统发育树。构建了突变HPr衍生物，其中调节性丝氨酸变为丙氨酸或天冬氨酸。将克隆的 galP 基因整合到枯草芽孢杆菌的染色体中，并证明该生物中突变HPr蛋白的合成可促进GalP的调控，这对于直接变构机制。因此，我们在没有其他方式表现出这种现象的生物体中重构了诱导剂控制。这些结果与 L中的诱导物排斥和驱除的结论一致。 brevis 通过多组分信号转导机制进行操作，其中糖酵解中间体（例如果糖1,6-双磷酸酯（细胞内效应物））的存在源自外源葡萄糖（细胞外效应物），可激活HPr（Ser）激酶（传感器）磷酸化Ser-46（信使）上的HPr，该蛋白与半乳糖：H + 转运蛋白（靶标）结合，导致糖转运与质子转运蛋白（反应）解偶联。这种级联使细菌能够快速响应外部糖浓度的变化。了解诱导剂控制的分子机制将使我们对细菌的代谢过程和运输过程之间的联系有所了解。

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