## 3 Results
### Screening of Downregulated Genes in DaMDHAR-Expressing Yeast Cells to FT2 Stress  
Compared with _DaMDHAR_-dependent upregulated genes, downregulated genes were identified in FT2 stress. Among the 135 downregulated genes, compared with WT cells, DM cells expressing _DaMDAHR_ decreased the expression of genes involved in protein processing in the endoplasmic reticulum (ER; _SWP1_), \(\alpha\)-glucose transport connected with glucose transport, sugar::proton symporter, \(\alpha\)-glucose transporter, and maltose metabolic process (_MAL31, MPH2_, and _HXT3_), respiratory electron transport chain (_AIF1_ and _COX2_), oxidoreductase activity using NAD(P)\({}^{+}\) as an acceptor (_TRX3_), pantotheane CoA biosynthesis (_ILV3_), selenocompound metabolism (_IRC7_), meiosis-dependent cell cycle combined with _HXT3_ and _MAM1_, ribosome biogenesis (_NAN1_), oxidative phosphorylation (_COX2_), and glycolysis/glucoseogenesis (_PDC6_), under FT2 stress (Figure 5; Table 2, Tables S2, S5, and S6). _COX2_ encoding cytochrome c oxidase was connected to the co-cluster of oxidative phosphorylation and respiratory electron chain (Figure 5). In particular, _MAM1_ (coding monopolin) and _HXT3_ (coding low-affinity glucose transporter) were downregulated in DM cells under FT2 stress, which was connected with meiosis regarding KEGG-based classification (Figure 5 and Table S6). In addition to _MAM1_ coding meiosis-specific kinetochore-associated protein, a low mRNA level of _HXT3_ provides a growth advantage for young daughters during mitosis or quiescence under FT2 stress, who better prepared for nutritional changes in FT2 stress. By contrast, other _HXT_ genes, such as _HXT2_ and _HXT4_ with high-affinity glucose transporter, were activated or unchanged during the mitosis or quiescence cell cycle under stress conditions, which led to glucose homeostasis. Thus, these results indicate that _DaMDHAR_-expressing DM cells could, at least partially, enhance the mitotic cell cycle with cell division or quiescence arrest, but not the meiosis-dependent cell cycle. With regard to the single gene, DM cells decreased the gene expression of _AIF1_ encoding mitochondrial cell death effector, _YNL190W_ encoding hydrophilic, _YPK2_ encoding putative protein kinase similar to S/T protein kinase Ypk1p, _VPS26_ encoding vacuolar protein sorting, _TRX3_ encoding mitochondrial thioredoxin, _SSH4_ encoding a specific factor required for ubiquitination, _HSP30_ encoding heat shock protein (HSP) 30, _COX2_ encoding cytochrome c oxidase subunit II, and _FDH2_ encoding NAD\({}^{*}\)--dependent formate dehydrogenase (Table 2 and Table S2). _HSP30_ expression was the highest low in DM cells (Table 2). In relation to organelles, DM cells downregulated the expression of genes related to functionality and metabolism of mitochondria (_ILV3_, _TRX3_, _COX2_, _AIF1_, and _OCD2_), PM (_ZEO1_, _MAL31_, _RIM19_, _MPH2_, _HXT3_, _HXT17_, _SMA1_, and _FSP30_), and CWI (_YNL190W_ and _NCW1_) (Table 2, Tables S2, S5, and S6). Regarding transcription factors, compared with WT cells, DM cells downregulated putative transcriptional activator (_MSN2_), zinc finger transcriptional repressor (_MIG2_), and _MGA1_ encoding protein similar to heat shock transcriptional factor under FT2 stress compared to WT cells (Table 2 and Table S2). By contrast, 70 genes encoding a hypothetical or uncharacterized protein decreased in DM cells under FT2 stress, and the expression of _YJL197-C_ was the lowest following that of _HSP30_ (Table 2 and Table S2). Thus, these results suggested that _DaMDHAR_ expression contributed to FT2-mediated stress response by regulating oxidative phosphorylation, selenocompound metabolism, cell cycle arrest, and ER and ribosomal functions via transcriptional activator and repressor.