Transcriptional remodeling in response to transfer upon carbon-limited or metformin-supplemented media in S. cerevisiae and its effect on chronological life span

Verfasser / Beitragende:
[Esra Borklu-Yucel, Serpil Eraslan, Kutlu Ulgen]
Ort, Verlag, Jahr:
2015
Enthalten in:
Applied Microbiology and Biotechnology, 99/16(2015-08-01), 6775-6789
Format:
Artikel (online)
ID: 60549830X
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024 7 0 |a 10.1007/s00253-015-6728-5  |2 doi 
035 |a (NATIONALLICENCE)springer-10.1007/s00253-015-6728-5 
245 0 0 |a Transcriptional remodeling in response to transfer upon carbon-limited or metformin-supplemented media in S. cerevisiae and its effect on chronological life span  |h [Elektronische Daten]  |c [Esra Borklu-Yucel, Serpil Eraslan, Kutlu Ulgen] 
520 3 |a One of the factors affecting chronological life span (CLS) in budding yeast is nutrient, especially carbon limitation. Aside from metabolites in the growth medium such as glucose, amino acids, and acetic acid, many pharmaceuticals have also been proven to alter CLS. Besides their impact on life span, these drugs are also prospective chemicals to treat the age-associated diseases, so the identification of their action mechanism and their potential side effects is of crucial importance. In this study, the effects of caloric restriction and metformin, a dietary mimetic pharmaceutical, on yeast CLS are compared. Saccharomyces cerevisiae cells grown in synthetic dextrose complete (SDC) up to mid-exponential phase were either treated with metformin or were subjected to glucose limitation. The impacts of these perturbations were analyzed via transcriptomics, and the common (stimulation of glucose uptake, induction of mitochondrial maintenance, and reduction of protein translation) and divergent (stimulation of aerobic respiration and reprogramming of respiratory electron transport chain (ETC)) cellular responses specific to each treatment were determined. These results revealed that both glucose limitation and metformin treatment stimulate CLS extension and involve the mitochondrial function, probably by creating an efficient mitochondria-to-nucleus signaling of either aerobic respiration or ETC signaling stimulation, respectively. 
540 |a Springer-Verlag Berlin Heidelberg, 2015 
690 7 |a Metformin  |2 nationallicence 
690 7 |a Carbon limitation  |2 nationallicence 
690 7 |a S. cerevisiae  |2 nationallicence 
690 7 |a Transcriptomics  |2 nationallicence 
690 7 |a Aerobic respiration  |2 nationallicence 
690 7 |a ETC  |2 nationallicence 
700 1 |a Borklu-Yucel  |D Esra  |u Department of Chemical Engineering, Bogazici University, Bebek, Istanbul, Turkey  |4 aut 
700 1 |a Eraslan  |D Serpil  |u Department of Chemical Engineering, Bogazici University, Bebek, Istanbul, Turkey  |4 aut 
700 1 |a Ulgen  |D Kutlu  |u Department of Chemical Engineering, Bogazici University, Bebek, Istanbul, Turkey  |4 aut 
773 0 |t Applied Microbiology and Biotechnology  |d Springer Berlin Heidelberg  |g 99/16(2015-08-01), 6775-6789  |x 0175-7598  |q 99:16<6775  |1 2015  |2 99  |o 253 
856 4 0 |u https://doi.org/10.1007/s00253-015-6728-5  |q text/html  |z Onlinezugriff via DOI 
898 |a BK010053  |b XK010053  |c XK010000 
900 7 |a Metadata rights reserved  |b Springer special CC-BY-NC licence  |2 nationallicence 
908 |D 1  |a research-article  |2 jats 
949 |B NATIONALLICENCE  |F NATIONALLICENCE  |b NL-springer 
950 |B NATIONALLICENCE  |P 856  |E 40  |u https://doi.org/10.1007/s00253-015-6728-5  |q text/html  |z Onlinezugriff via DOI 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Borklu-Yucel  |D Esra  |u Department of Chemical Engineering, Bogazici University, Bebek, Istanbul, Turkey  |4 aut 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Eraslan  |D Serpil  |u Department of Chemical Engineering, Bogazici University, Bebek, Istanbul, Turkey  |4 aut 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Ulgen  |D Kutlu  |u Department of Chemical Engineering, Bogazici University, Bebek, Istanbul, Turkey  |4 aut 
950 |B NATIONALLICENCE  |P 773  |E 0-  |t Applied Microbiology and Biotechnology  |d Springer Berlin Heidelberg  |g 99/16(2015-08-01), 6775-6789  |x 0175-7598  |q 99:16<6775  |1 2015  |2 99  |o 253