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首页> 外文期刊>Applied Microbiology >Inhibitory Role of Greatwall-Like Protein Kinase Rim15p in Alcoholic Fermentation via Upregulating the UDP-Glucose Synthesis Pathway in Saccharomyces cerevisiae
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Inhibitory Role of Greatwall-Like Protein Kinase Rim15p in Alcoholic Fermentation via Upregulating the UDP-Glucose Synthesis Pathway in Saccharomyces cerevisiae

机译：长城样蛋白激酶Rim15p在酿酒酵母中通过上调酿酒酵母的UDP葡萄糖合成途径的抑制作用。

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The high fermentation rate of Saccharomyces cerevisiae sake yeast strains is attributable to a loss-of-function mutation in the RIM15 gene, which encodes a Greatwall-family protein kinase that is conserved among eukaryotes. In the present study, we performed intracellular metabolic profiling analysis and revealed that deletion of the RIM15 gene in a laboratory strain impaired glucose-anabolic pathways through the synthesis of UDP-glucose (UDPG). Although Rim15p is required for the synthesis of trehalose and glycogen from UDPG upon entry of cells into the quiescent state, we found that Rim15p is also essential for the accumulation of cell wall β-glucans, which are also anabolic products of UDPG. Furthermore, the impairment of UDPG or 1,3-β-glucan synthesis contributed to an increase in the fermentation rate. Transcriptional induction of PGM2 (phosphoglucomutase) and UGP1 (UDPG pyrophosphorylase) was impaired in Rim15p-deficient cells in the early stage of fermentation. These findings demonstrate that the decreased anabolism of glucose into UDPG and 1,3-β-glucan triggered by a defect in the Rim15p-mediated upregulation of PGM2 and UGP1 redirects the glucose flux into glycolysis. Consistent with this, sake yeast strains with defective Rim15p exhibited impaired expression of PGM2 and UGP1 and decreased levels of β-glucans, trehalose, and glycogen during sake fermentation. We also identified a sake yeast-specific mutation in the glycogen synthesis-associated glycogenin gene GLG2 , supporting the conclusion that the glucose-anabolic pathway is impaired in sake yeast. These findings demonstrate that downregulation of the UDPG synthesis pathway is a key mechanism accelerating alcoholic fermentation in industrially utilized S. cerevisiae sake strains.
机译：酿酒酵母酵母菌株的高发酵率归因于RIM15基因的功能丧失突变，该基因编码真核生物中保守的长城家族蛋白激酶。在本研究中，我们进行了细胞内代谢谱分析，并揭示了实验室菌株中RIM15基因的缺失通过UDP-葡萄糖（UDPG）的合成损害了葡萄糖-代谢途径。尽管Rim15p是细胞进入静止状态后从UDPG合成海藻糖和糖原所必需的，但我们发现Rim15p对于细胞壁β-葡聚糖的积累也是必不可少的，后者也是UDPG的合成代谢产物。此外，UDPG或1，3-β-葡聚糖合成的损伤导致发酵速率的增加。在发酵的早期阶段，在Rim15p缺陷型细胞中，PGM2（磷酸葡萄糖变位酶）和UGP1（UDPG焦磷酸化酶）的转录诱导受损。这些发现表明，由Rim15p介导的PGM2和UGP1上调缺陷引发的葡萄糖向UDPG和1,3-β-葡聚糖的合成代谢降低，使葡萄糖通量重新定向到糖酵解中。与此相一致，具有Rim15p缺陷的清酒酵母菌株在清酒发酵过程中表现出PGM2和UGP1的表达受损，并且β-葡聚糖，海藻糖和糖原的水平降低。我们还在糖原合成相关的糖原蛋白基因GLG2中鉴定了一种清酒酵母特有的突变，支持了清酒酵母中葡萄糖代谢途径受损的结论。这些发现表明，在工业利用的酿酒酵母中，UDPG合成途径的下调是加速酒精发酵的关键机制。

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