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In this work we evaluated the impact of nutritional unbalances, as lipids/nitrogen unbalances, on wine yeast survival during alcoholic fermentation. We showed that lipids limitations (actually ergosterol limitation) lead to a rapid loss of viability during the stationary phase of fermentation but that cell death rate is strongly modulated by the amount of nitrogen sources. Yeast survival is reduced when an excess of nitrogen is available in lipid-limited fermentations. Such rapid dying yeast cells fermenting with high nitrogen level and lipids-limited amounts displayed a low storage of carbohydrate trehalose and glycogen compared to nitrogen limited cells. Consistently, examination of the cells stress response using an HSP12 promoter-driven GFP expression showed that lipids limitation triggered a weaker stress response than nitrogen limitation. We examined the involvement of nitrogen signalling pathway in the triggering of cell death using a sch9-deleted strain. We showed that deletion of SCH9 restored a high yeast viability indicating that the signaling pathway acting through Sch9p is involved in the enhanced cell death triggered by nitrogen excess. In addition we showed that various nitrogen sources provoked cell death but that histidine and proline did not trigger a similar effect. As a whole our data indicate that lipids limitation does not elicit a transcriptional program leading to a stress response which protects yeast cells and that nitrogen excess triggers cell death through a modulation of this stress response, but not by HSP12. These results point a potential negative role of nitrogen in fermentation which has until now never been described and taken into account in the management of alcoholic fermentations. 2 conditions with 2 biological replicates compared: 59A and 59A-Sch9

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