Biopolym. Cell. 2014; 30(5):358-364.
Genomics, Transcriptomics and Proteomics
Sensitivity of Saccharomyces cerevisiae defective in TOR signaling pathway to carbonyl/oxidative stress
1Valishkevych B. V.
  1. Vassyl Stefanyk Precarpathian National University
    57, Shevchenko Str., Ivano-Frankivsk, Ukraine, 76018

Abstract

Aim. To investigate the influence of carbonyl/oxidative stress induced by glyoxal, methylglyoxal and hydrogen peroxide on the survival of Saccharomyces cerevisiae, defective for different parts of TOR- signaling pathway, grown on glucose or fructose. Methods. The assessment of number of colony-forming units to determine the yeast reproductive ability. Results. It was shown that at certain concentrations the mentioned above toxicants caused an increase in yeast survival, indicating the hormetic effect. Conclusions. The TOR signaling pathway is involved in the hormetic effect, but it is specific for each strain and depends on the type of carbohydrate in the incubation medium.
Keywords: Saccharomyces cerevisiae, glucose, fructose, TOR-signaling pathway, carbonyl/oxidative stress

References

[1] Laplante M, Sabatini DM. mTOR signaling in growth control and disease. Cell. 2012;149(2):274-93.
[2] Heitman J, Movva NR, Hall MN. Targets for cell cycle arrest by the immunosuppressant rapamycin in yeast. Science. 1991;253(5022):905-9.
[3] Lushchak VI. Budding yeast Saccharomyces cerevisiae as a model to study oxidative modification of proteins in eukaryotes. Acta Biochim Pol. 2006;53(4):679-84.
[4] Fontana L, Partridge L, Longo VD. Extending healthy life span--from yeast to humans. Science. 2010;328(5976):321-6.
[5] Rockenfeller P, Madeo F. Ageing and eating. Biochim Biophys Acta. 2010;1803(4):499-506.
[6] Summers DW, Cyr DM. Use of yeast as a system to study amyloid toxicity. Methods. 2011;53(3):226-31.
[7] Kunz J, Henriquez R, Schneider U, Deuter-Reinhard M, Movva NR, Hall MN. Target of rapamycin in yeast, TOR2, is an essential phosphatidylinositol kinase homolog required for G1 progression. Cell. 1993;73(3):585-96.
[8] Cafferkey R, Young PR, McLaughlin MM, Bergsma DJ, Koltin Y, Sathe GM, Faucette L, Eng WK, Johnson RK, Livi GP. Dominant missense mutations in a novel yeast protein related to mammalian phosphatidylinositol 3-kinase and VPS34 abrogate rapamycin cytotoxicity. Mol Cell Biol. 1993;13(10):6012-23.
[9] Warburg O, Posener K, Negelein E. Uber den stoffwechsel der carcinomzelle. Die Naturheilkunde. 1924;152:309–44.
[10] Weinberg RA. The molecular basis of oncogenes and tumor suppressor genes. Ann N Y Acad Sci. 1995;758:331-8.
[11] Laplante M, Sabatini DM. mTOR signaling at a glance. J Cell Sci. 2009;122(Pt 20):3589-94.
[12] Bierer BE, Jin YJ, Fruman DA, Calvo V, Burakoff SJ. FK 506 and rapamycin: molecular probes of T-lymphocyte activation. Transplant Proc. 1991;23(6):2850-5.
[13] Sarbassov DD, Ali SM, Sabatini DM. Growing roles for the mTOR pathway. Curr Opin Cell Biol. 2005;17(6):596-603.
[14] V?zina C, Kudelski A, Sehgal SN. Rapamycin (AY-22,989), a new antifungal antibiotic. I. Taxonomy of the producing streptomycete and isolation of the active principle. J Antibiot (Tokyo). 1975;28(10):721-6.
[15] Efeyan A, Zoncu R, Sabatini DM. Amino acids and mTORC1: from lysosomes to disease. Trends Mol Med. 2012;18(9):524-33.
[16] Appenzeller-Herzog C, Hall MN. Bidirectional crosstalk between endoplasmic reticulum stress and mTOR signaling. Trends Cell Biol. 2012;22(5):274-82.
[17] Ha CW, Huh WK. Rapamycin increases rDNA stability by enhancing association of Sir2 with rDNA in Saccharomyces cerevisiae. Nucleic Acids Res. 2011;39(4):1336-50.
[18] Medvedik O, Lamming DW, Kim KD, Sinclair DA. MSN2 and MSN4 link calorie restriction and TOR to sirtuin-mediated lifespan extension in Saccharomyces cerevisiae. PLoS Biol. 2007;5(10):e261.
[19] Brant JM, Beck S, Dudley WN, Cobb P, Pepper G, Miaskowski C. Symptom trajectories in posttreatment cancer survivors. Cancer Nurs. 2011;34(1):67-77.
[20] Crespo JL, Hall MN. Elucidating TOR signaling and rapamycin action: lessons from Saccharomyces cerevisiae. Microbiol Mol Biol Rev. 2002;66(4):579-91.
[21] Beck T, Hall MN. The TOR signalling pathway controls nuclear localization of nutrient-regulated transcription factors. Nature. 1999;402(6762):689-92.
[22] Semchyshyn H. Hydrogen peroxide-induced response in E. coli and S. cerevisiae: different stages of the flow of the genetic information. Cent Eur J Biol. 2009; 4(2):142–53.
[23] Robida-Stubbs S, Glover-Cutter K, Lamming DW, Mizunuma M, Narasimhan SD, Neumann-Haefelin E, Sabatini DM, Blackwell TK. TOR signaling and rapamycin influence longevity by regulating SKN-1/Nrf and DAF-16/FoxO. Cell Metab. 2012;15(5):713-24.
[24] Semchyshyn HM. Hormetic concentrations of hydrogen peroxide but not ethanol induce cross-adaptation to different stresses in budding yeast. Int J Microbiol. 2014;2014:485792.
[25] Lushchak VI. Dissection of the hormetic curve: analysis of components and mechanisms. Dose Response. 2014;12(3):466-79.
[26] Bayliak MM, Burdyliuk NI, Izers'ka LI, Lushchak VI. Concentration-Dependent Effects of Rhodiola Rosea on Long-Term Survival and Stress Resistance of Yeast Saccharomyces Cerevisiae: The Involvement of YAP 1 and MSN2/4 Regulatory Proteins. Dose Response. 2013;12(1):93-109.
[27] Mirisola MG, Longo VD. A radical signal activates the epigenetic regulation of longevity. Cell Metab. 2013;17(6):812-3.
[28] Cornelius C, Perrotta R, Graziano A, Calabrese EJ, Calabrese V. Stress responses, vitagenes and hormesis as critical determinants in aging and longevity: Mitochondria as a "chi". Immun Ageing. 2013;10(1):15.
[29] Ljungdahl PO, Daignan-Fornier B. Regulation of amino acid, nucleotide, and phosphate metabolism in Saccharomyces cerevisiae. Genetics. 2012;190(3):885-929.
[30] Semchyshyn HM, Lozinska LM, Miedzobrodzki J, Lushchak VI. Fructose and glucose differentially affect aging and carbonyl/oxidative stress parameters in Saccharomyces cerevisiae cells. Carbohydr Res. 2011;346(7):933-8.
[31] Semchyshyn HM, Lozinska LM. Fructose protects baker's yeast against peroxide stress: potential role of catalase and superoxide dismutase. FEMS Yeast Res. 2012;12(7):761-73.
[32] Helliwell SB, Howald I, Barbet N, Hall MN. TOR2 is part of two related signaling pathways coordinating cell growth in Saccharomyces cerevisiae. Genetics. 1998;148(1):99-112.
[33] Meynel J. Meynell GG, Meynell E. Experimental microbiology (Theory and Practice). Moscow, Mir, 1967; 347 p.
[34] Semchyshyn HM. Reactive carbonyl species in vivo: generation and dual biological effects. ScientificWorldJournal. 2014;2014:417842.
[35] Semchyshyn HM. Fructation in vivo: detrimental and protective effects of fructose. Biomed Res Int. 2013;2013:343914.
[36] Semchyshyn HM, Lushchak VI. Interplay between oxidative and carbonyl stresses: molecular mechanisms, biological effects and therapeutic strategies of protection. Oxidative Stress – Molecular mechanisms and biological effects. InTech. 2012; 15–46.
[37] Lozins'ka LM, Semchyshyn HM. Biological aspects of non-enzymatic glycosylation. Ukr Biokhim Zh. 2012;84(5):16-37.
[38] Semchyshyn HM, Bayliak MM, Lushchak VI. Starvation in yeasts: biochemical aspects. Biology of starvation in humans and other organisms. Ed. TC. Merkin. New York, Nova Science, 2011;103–50.
[39] Homza BV, Vasyl'kovs'ka RA, Semchyshyn HM. Defects in TOR regulatory complexes retard aging and carbonyl/oxidative stress development in yeast Saccharomyces cerevisiae. Ukr Biokhim Zh. 2014;86(1):85-92.
[40] Lushchak VI. Oxidative stress and mechanisms of protection against it in bacteria. Biochemistry (Mosc). 2001;66(5):476-89.
[41] Semchyshyn HM. Defects in antioxidant defence enhance glyoxal toxicity in the yeast Saccharomyces cerevisiae. Ukr Biokhim Zh. 2013;85(5):50-60.
[42] Turk Z. Glycotoxines, carbonyl stress and relevance to diabetes and its complications. Physiol Res. 2010;59(2):147-56.
[43] Kalapos MP. Methylglyoxal in living organisms: chemistry, biochemistry, toxicology and biological implications. Toxicol Lett. 1999;110(3):145-75.
[44] Richard JP. Mechanism for the formation of methylglyoxal from triosephosphates. Biochem Soc Trans. 1993;21(2):549-53.