Effect of Ethanol on Cell Growth of Budding Yeast: Genes That Are Important for Cell Growth in the Presence of Ethanol

Kubota, Shunsuke; Takeo, Ikuko; Kume, Kazunori; Kanai, Masayuki; Shitamukai, Atsunori; Mizunuma, Masaki; Miyakawa, Tokichi; Shimoi, Hitoshi; Iefuji, Haruyuki; Hirata, Dai

doi:10.1271/bbb.68.968

Cited by 146 publications

(152 citation statements)

References 10 publications

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“…Fusel alcohol, butanol, chlorpromazine 4 and isoflurane inhibit translation initiation in yeast (Ashe et al, 2001;Deloche et al, 2004;Palmer et al, 2005), whereas ethanol 16 depolarizes the actin cytoskeleton (Kubota et al, 2004). Recently we found that local anesthetics, antipsychotic phenothiazines and cationic surfactants rapidly shut down both translation initiation and actin polarization in yeast, whereas anionic surfactants shut down only actin polarization without apparent shutdown of translation initiation, similar to the above shutdowns observed in the stresses (b, c) (Araki et al, 2005;Uesono et al, 2008).…”

Section: Y Uesono Et Alsupporting

confidence: 56%

Structural analysis of compounds with actions similar to local anesthetics and antipsychotic phenothiazines in yeast

Uesono¹,

Toh‐e²,

Kikuchi³

et al. 2011

Yeast

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Local anesthetics and antipsychotic phenothiazines cause a rapid shutdown of both actin polarization and translation initiation in yeast cells, like some environmental stresses. These compounds all have an amphiphilic structure, surfactant activity and the ability to lyse yeast cells. To elucidate the structures responsible for the shutdown activity and cell lysis, we investigated a variety of amphiphiles. In the hydrophobic region, the straight alkyl structure was sufficient for the shutdown of actin polarization and translational initiation. In the hydrophilic region of the straight alkyl compounds, cationic trimethyl ammonium (TMA) and non-ionic hydroxyl structure (alcohols) shut down both reactions, while an anionic structure, sulphate, with a long alkyl chain (≥C6) shut down actin polarization only. On the compounds that shut down both reactions, including the clinical drugs, TMA compounds and alcohols, the potencies of shutdown and lysis exponentially increased with increasing the number of carbons in the hydrophobic region, whereas safety was affected by the structures of both hydrophilic and hydrophobic regions. These results indicate that the yeast system can easily evaluate clinical drugs, and provide a structural basis for designing compounds to shut down intracellular reactions.

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Section: Y Uesono Et Alsupporting

confidence: 56%

Structural analysis of compounds with actions similar to local anesthetics and antipsychotic phenothiazines in yeast

Uesono¹,

Toh‐e²,

Kikuchi³

et al. 2011

Yeast

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“…In previous studies, Adr1 was shown to bind the promoters for 14 different genes involved in the generation of acetyl-CoA and NADH from nonfermentable substrates (42, 43; (24). The increase in cell size seen in ethanol-grown cells is due to a delay in the cell cycle that is partially mediated by the tyrosine kinase Swe1, a negative regulator of the Cdc28-Clb complexes (24). Since Ats1p regulates the activity of the same complex, we propose that Adr1 FIG.…”

Section: Discussionmentioning

confidence: 99%

Gene Set Coregulated by the Saccharomyces cerevisiae Nonsense-Mediated mRNA Decay Pathway

et al. 2005

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The nonsense-mediated mRNA decay (NMD) pathway has historically been thought of as an RNA surveillance system that degrades mRNAs with premature translation termination codons, but the NMD pathway of Saccharomyces cerevisiae has a second role regulating the decay of some wild-type mRNAs. In S. cerevisiae, a significant number of wild-type mRNAs are affected when NMD is inactivated. These mRNAs are either wild-type NMD substrates or mRNAs whose abundance increases as an indirect consequence of NMD. A current challenge is to sort the mRNAs that accumulate when NMD is inactivated into direct and indirect targets. We have developed a bioinformatics-based approach to address this challenge. Our approach involves using existing genomic and function databases to identify transcription factors whose mRNAs are elevated in NMD-deficient cells and the genes that they regulate. Using this strategy, we have investigated a coregulated set of genes. We have shown that NMD regulates accumulation of ADR1 and GAL4 mRNAs, which encode transcription activators, and that Adr1 is probably a transcription activator of ATS1. This regulation is physiologically significant because overexpression of ADR1 causes a respiratory defect that mimics the defect seen in strains with an inactive NMD pathway. This strategy is significant because it allows us to classify the genes regulated by NMD into functionally related sets, an important step toward understanding the role NMD plays in the normal functioning of yeast cells.Nonsense-mediated mRNA decay (NMD) is a highly conserved mRNA degradation pathway. Historically, NMD has been thought of as an RNA surveillance system whose role is to identify and rid cells of mRNA with premature termination codons and thus prevents accumulation of potentially harmful truncated proteins. However, more recently, it has become apparent that the NMD pathway of Saccharomyces cerevisiae has a second role regulating the decay of wild-type mRNAs.Genome-wide transcription profiling has revealed that a significant number (estimated to be between 5 and 10%) of wildtype transcripts accumulate in yeast cells when the NMD pathway is inactivated (15, 28). These mRNAs that accumulate can be direct NMD substrates or could accumulate as an indirect consequence of inactivation of NMD. PPR1 and URA3 mRNAs represent examples of mRNAs that are directly and indirectly affected by inactivation of the NMD pathway, respectively. PPR1 mRNA is an NMD substrate because it is degraded more rapidly in cells with an active NMD pathway than those in which the NMD pathway has been inactivated (20). It encodes a transcription activator, and the genes activated by Ppr1 are up-regulated in cells with an inactive NMD pathway (18,27). For example, URA3 is regulated by Ppr1. URA3 mRNA accumulates in cells with an inactive NMD pathway; however, URA3 mRNA has the same half-life in cells with active and inactive NMD pathways (27). Thus, accumulation of URA3 mRNA is due to increased transcription activation by Ppr1 as an indirect consequence of inactiv...

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“…External stresses shown to act in this manner include hyperosmotic shock (Lew and Reed 1995;Sia et al 1998;Alexander et al 2001), exposure to high concentrations of ethanol (Kubota et al 2004), nutrient depletion (Uesono et al 2004), and even physical constraint of cells in microfabricated chambers (Suzuki et al 2004). In all of these cases, the stresses lead to depolarization of the actin cytoskeleton.…”

Section: Regulation Of Cdc28p Tyrosine Phosphorylation In Response Tomentioning

confidence: 99%

“…Actin organization: Many physiological stresses that occur frequently in the yeast's natural environment (e.g., changing temperature, osmolarity, nutrient level, or ethanol concentration) cause a transient depolarization of the actin cytoskeleton (Chowdhury et al 1992;Lillie and Brown 1994;Kubota et al 2004;Uesono et al 2004). This is thought to represent an adaptive response that allows the cell to adjust to the altered environment before engaging in polarized growth (Delley and Hall 1999;Keaton and Lew 2006).…”

Section: Regulation Of Cdc28p Tyrosine Phosphorylation In Response Tomentioning

confidence: 99%

Morphogenesis and the Cell Cycle

2012

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Studies of the processes leading to the construction of a bud and its separation from the mother cell in Saccharomyces cerevisiae have provided foundational paradigms for the mechanisms of polarity establishment, cytoskeletal organization, and cytokinesis. Here we review our current understanding of how these morphogenetic events occur and how they are controlled by the cellcycle-regulatory cyclin-CDK system. In addition, defects in morphogenesis provide signals that feed back on the cyclin-CDK system, and we review what is known regarding regulation of cell-cycle progression in response to such defects, primarily acting through the kinase Swe1p. The bidirectional communication between morphogenesis and the cell cycle is crucial for successful proliferation, and its study has illuminated many elegant and often unexpected regulatory mechanisms. Despite considerable progress, however, many of the most puzzling mysteries in this field remain to be resolved.

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Effect of Ethanol on Cell Growth of Budding Yeast: Genes That Are Important for Cell Growth in the Presence of Ethanol

Cited by 146 publications

References 10 publications

Structural analysis of compounds with actions similar to local anesthetics and antipsychotic phenothiazines in yeast

Structural analysis of compounds with actions similar to local anesthetics and antipsychotic phenothiazines in yeast

Gene Set Coregulated by the Saccharomyces cerevisiae Nonsense-Mediated mRNA Decay Pathway

Morphogenesis and the Cell Cycle

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