INRA, UMR1083, Montpellier, France.
PLoS One. 2013 Apr 26;8(4):e61645. doi: 10.1371/journal.pone.0061645. Print 2013.
We evaluated the consequences of nutritional imbalances, particularly lipid/nitrogen imbalances, on wine yeast survival during alcoholic fermentation. We report that lipid limitation (ergosterol limitation in our model) led to a rapid loss of viability during the stationary phase of fermentation and that the cell death rate is strongly modulated by nitrogen availability and nature. Yeast survival was reduced in the presence of excess nitrogen in lipid-limited fermentations. The rapidly dying yeast cells in fermentations in high nitrogen and lipid-limited conditions displayed a lower storage of the carbohydrates trehalose and glycogen than observed in nitrogen-limited cells. We studied the cell stress response using HSP12 promoter-driven GFP expression as a marker, and found that lipid limitation triggered a weaker stress response than nitrogen limitation. We used a SCH9-deleted strain to assess the involvement of nitrogen signalling pathways in the triggering of cell death. Deletion of SCH9 increased yeast viability in the presence of excess nitrogen, indicating that a signalling pathway acting through Sch9p is involved in this nitrogen-triggered cell death. We also show that various nitrogen sources, but not histidine or proline, provoked cell death. Our various findings indicate that lipid limitation does not elicit a transcriptional programme that leads to a stress response protecting yeast cells and that nitrogen excess triggers cell death by modulating this stress response, but not through HSP12. These results reveal a possibly negative role of nitrogen in fermentation, with reported effects referring to ergosterol limitation conditions. These effects should be taken into account in the management of alcoholic fermentations.
我们评估了营养失衡,特别是脂质/氮失衡,对酒精发酵过程中葡萄酒酵母存活的影响。我们报告称,脂质限制(我们模型中的麦角固醇限制)导致发酵静止期的活力迅速丧失,细胞死亡率受氮供应和氮源性质的强烈调节。在脂质限制发酵中存在过量氮时,酵母存活率降低。在高氮和脂质限制条件下快速死亡的酵母细胞,其碳水化合物海藻糖和糖原的储存量低于氮限制细胞。我们使用 HSP12 启动子驱动 GFP 表达作为标记来研究细胞应激反应,发现脂质限制比氮限制触发的应激反应更弱。我们使用 SCH9 缺失菌株来评估氮信号通路在触发细胞死亡中的作用。SCH9 的缺失增加了过量氮存在时酵母的存活率,表明通过 Sch9p 作用的信号通路参与了这种氮触发的细胞死亡。我们还表明,各种氮源,但不是组氨酸或脯氨酸,引发了细胞死亡。我们的各种发现表明,脂质限制不会引发导致酵母细胞应激反应保护的转录程序,并且氮过量通过调节这种应激反应而不是通过 HSP12 触发细胞死亡。这些结果揭示了氮在发酵过程中可能起负面作用,报告的影响与麦角固醇限制条件有关。在管理酒精发酵时,应考虑到这些影响。