7th Iranian Congress Of Clinical Microbiology, Iran, 1 - 04 October 2013, pp.72
Conference Paper / Summary Text
Introduction and Objectives: Since Schizosaccharomyces pombe has homologous of many human genes, it offers advantages for investigation of molecular mechanisms underlying human disease. Hyperglycemia-induced oxidative stress also is the known cause of diabetes complications. We aimed to investigate oxidative stress response in a mutant strain of S.pombe resistant to glucose repression (ird11) and impact of glucose signaling/ transport on it.
Materials and Methods: Wild type S.pombe Lindner Liquifacience (972 h-) andird11mutant were used.Ird11 mutant was grown in selective medium consisting of 0.5% yeast extract, 3% sucrose and 400 μg/ml 2-deoxy-D-glucose.The wild type and ird11 were cultured in standard rich medium (YEL).Induction of oxidative stress, cell-disruption and RNA-isolation were performed.DNA Microarray was prepared according to Nimble Gene (GenMar), Izmir, Turkey.
Results: Hsp16’s expression level is decreased in ird11in which elevated levels of glucose is taken by cells. Hsp16 is induced by deoxy ribo nucleotide depletion or DNA damage. We have previously shown that intracellular oxidation level in ird11 is significantly lower than that of wild type. Our microarray results revealed hsp16 expression level is decreased by (x-3.6) in ird11 compared to wild type. Another finding was sharp increase (x2.068) in ureidoglycolate hydrolase expression level.
Conclusion: 1)- According to these data, although hsp16 is downstream of Atf1, in response to oxidative stress, its expression is not regulated through Sty1 MAPK pathway suggesting possibility of another pathway.2)- As cells utilize purine bases as nitrogen source in nitrogen limited conditions, maybe overproduction of CoQ10 plays a pivotal role in natural response to hyperglycemia-induced oxidative stress in ird11.
Keywords: Hyperglycemia-induced oxidative stress, Hsp16, CoQ10, Schizosaccharomyces pombe.