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首页> 外文期刊>Applied Microbiology >Regulation of Dual Glycolytic Pathways for Fructose Metabolism in Heterofermentative Lactobacillus panis PM1
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Regulation of Dual Glycolytic Pathways for Fructose Metabolism in Heterofermentative Lactobacillus panis PM1

机译：双重糖酵解途径对异源发酵性潘氏乳杆菌PM1中果糖代谢的调控

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Lactobacillus panis PM1 belongs to the group III heterofermentative lactobacilli that use the 6-phosphogluconate/phosphoketolase (6-PG/PK) pathway as their central metabolic pathway and are reportedly unable to grow on fructose as a sole carbon source. We isolated a variant PM1 strain capable of sporadic growth on fructose medium and observed its distinctive characteristics of fructose metabolism. The end product pattern was different from what is expected in typical group III lactobacilli using the 6-PG/PK pathway (i.e., more lactate, less acetate, and no mannitol). In addition, in silico analysis revealed the presence of genes encoding most of critical enzymes in the Embden-Meyerhof (EM) pathway. These observations indicated that fructose was metabolized via two pathways. Fructose metabolism in the PM1 strain was influenced by the activities of two enzymes, triosephosphate isomerase (TPI) and glucose 6-phosphate isomerase (PGI). A lack of TPI resulted in the intracellular accumulation of dihydroxyacetone phosphate (DHAP) in PM1, the toxicity of which caused early growth cessation during fructose fermentation. The activity of PGI was enhanced by the presence of glyceraldehyde 3-phosphate (GAP), which allowed additional fructose to enter into the 6-PG/PK pathway to avoid toxicity by DHAP. Exogenous TPI gene expression shifted fructose metabolism from heterolactic to homolactic fermentation, indicating that TPI enabled the PM1 strain to mainly use the EM pathway for fructose fermentation. These findings clearly demonstrate that the balance in the accumulation of GAP and DHAP determines the fate of fructose metabolism and the activity of TPI plays a critical role during fructose fermentation via the EM pathway in L. panis PM1.
机译：潘氏乳杆菌PM1属于III类异发酵乳杆菌，其使用6-磷酸葡萄糖酸/磷酸脂酶（6-PG / PK）途径作为其中心代谢途径，并且据报道无法以果糖作为唯一碳源生长。我们分离出了能够在果糖培养基上零星生长的变异PM1菌株，并观察了果糖代谢的独特特征。最终产品模式与使用6-PG / PK途径的典型III组乳杆菌所期望的不同（即，乳酸更多，乙酸更少，无甘露醇）。此外，计算机分析表明，在Embden-Meyerhof（EM）途径中存在编码大多数关键酶的基因。这些观察结果表明果糖是通过两种途径代谢的。 PM1菌株中的果糖代谢受到两种酶（磷酸三糖异构酶（TPI）和葡萄糖6-磷酸异构酶（PGI））的影响。 TPI的缺乏导致PM1在细胞内积累磷酸二羟基丙酮磷酸酯（DHAP），其毒性导致果糖发酵过程中早期生长停止。 3-磷酸​​甘油醛（GAP）的存在增强了PGI的活性，甘油三醛（GAP）可使其他果糖进入6-PG / PK途径，从而避免DHAP的毒性。外源TPI基因表达使果糖代谢从杂乳酸发酵转变为纯乳酸发酵，这表明TPI使PM1菌株主要利用EM途径进行果糖发酵。这些发现清楚地表明，GAP和DHAP积累的平衡决定了果糖代谢的命运，TPI的活性在通过EM途径在潘氏乳酸杆菌PM1中进行果糖发酵过程中起着至关重要的作用。

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