Sugar-Induced Cell Death in the Yeast <i>S. cerevisiae</i> Is Accompanied by the Release of Octanoic Acid, Which Does Not Originate from the Fatty Acid Synthesis Type II Mitochondrial System
2023
Alexander Avtukh | Boris Baskunov | Varlam Keshelava | Airat Valiakhmetov
Incubation of the yeast <i>S. cerevisiae</i> with glucose, in the absence of other nutrients, leads to Sugar-Induced Cell Death (SICD), accompanied by the accumulation of Reactive Oxygen Species (ROS). Yeast acidifies the environment during glucose metabolism not only as a result of the activity of the H<sup>+</sup>-ATPase of the plasma membrane but also due to the release of carboxylic acids. Acetic acid is known to induce apoptosis in growing yeast. We analyzed the composition of the incubation medium and found octanoic acid (OA) but no other carboxylic acids. Its concentration (0.675 µM) was significantly lower than the one at which OA had a toxic effect on the cell. However, the theoretically calculated concentration of OA inside the cell (about 200 μM) was found to be high enough to lead to cell necrosis. To test the hypothesis that OA might cause SICD, we used a Δ<i>ACP1</i> strain incapable of synthesizing OA in the yeast mitochondrial Fatty Acid Synthesis type II system (FAS-II). The deletion of the <i>ACP1</i> gene did not affect the OA content in the medium. But, on the other hand, OA is a precursor of lipoic acid, which has antioxidant properties. However, strains with deleted genes for lipoic acid biosynthesis from OA (Δ<i>PPT2</i>, Δ<i>LIP2</i>, Δ<i>LIP5</i>, and Δ<i>SGV3</i>) showed no change in ROS and SICD levels. Thus, lipoic acid synthesized in FAS-II does not protect cells from ROS accumulated during SICD. We conclude that OA synthesized in the mitochondrial FAS-II system and its derivative lipoic acid are not involved in SICD in yeast <i>S. cerevisiae</i>.
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