Acid stress adaptation protects Saccharomyces cerevisiae from acetic acid-induced programmed cell death

被引:113
作者
Giannattasio, S
Guaragnella, N
Corte-Real, M
Passarella, S
Marra, E
机构
[1] CNR, Ist Biomembrane & Bioenerget, I-70126 Bari, Italy
[2] Univ Minho, Sch Sci, Dept Biol, Braga, Portugal
[3] Univ Molise, Dipartimento Sci Salute, Campobasso, Italy
关键词
Saccharomyces cerevisiae; programmed cell death; strong acid stress; superoxide dismutase; catalase;
D O I
10.1016/j.gene.2005.03.030
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
In this work evidence is presented that acid stress adaptation protects Saccharomyces cerevisiae from acetic acid-mediated programmed cell death. Exponential-phase yeast cells, non-adapted or adapted to acid stress by 30 min incubation in rich medium set at pH 3.0 with HCl, have been exposed to increasing concentrations of acetic acid and time course changes of cell viability have been assessed. Adapted cells, in contrast to non-adapted cells, when exposed to 80 mM acetic acid for 200 min did not display loss of cell viability associated to morphological alterations typical of apoptosis. Thus, 80 mM acetic acid death-inducing conditions were selected to further characterize the early molecular events leading to such active cell death process. Catalase was specifically activated during acid stress adaptation and protection against acetic acid-induced death was associated with maintenance of its activity during treatment with 80 MM acetic acid. On the other hand, intracellular superoxide dismutase activity was found present at comparable levels both in adapted and in dying yeast cells, excepting in non-adapted cells which displayed a maximum activity value after 15 min acetic acid exposure, corresponding to more than 80% cell viability. This study gives first experimental evidence that H2O2, rather than superoxide, detoxification may have a major role in preventing yeast cell death in response to acetic acid. The results, as a whole, suggest that commitment of S. cerevisiae to a programmed cell death process in response to acetic acid is mediated through a ROS-dependent apoptotic pathway. (c) 2005 Elsevier B.V. All rights reserved.
引用
收藏
页码:93 / 98
页数:6
相关论文
共 31 条
[1]   Ways of dying: multiple pathways to apoptosis [J].
Adams, JM .
GENES & DEVELOPMENT, 2003, 17 (20) :2481-2495
[2]   The origin of programmed cell death [J].
Ameisen, JC .
SCIENCE, 1996, 272 (5266) :1278-1279
[3]   Mitochondrial signaling: The retrograde response [J].
Butow, RA ;
Avadhani, NG .
MOLECULAR CELL, 2004, 14 (01) :1-15
[4]   Mitochondrial Hsp60, resistance to oxidative stress, and the labile iron pool are closely connected in Saccharomyces cerevisiae [J].
Cabiscol, E ;
Bellí, G ;
Tamarit, J ;
Echave, P ;
Herrero, E ;
Ros, J .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (46) :44531-44538
[5]   Activity of plasma membrane H+-ATPase and expression of PMA1 and PMA2 genes in Saccharomyces cerevisiae cells grown at optimal and low pH [J].
Carmelo, V ;
Bogaerts, P ;
SaCorreia, I .
ARCHIVES OF MICROBIOLOGY, 1996, 166 (05) :315-320
[6]   Effect of extracellular acidification on the activity of plasma membrane ATPase and on the cytosolic and vacuolar pH of Saccharomyces cerevisiae [J].
Carmelo, V ;
Santos, H ;
SaCorreia, I .
BIOCHIMICA ET BIOPHYSICA ACTA-BIOMEMBRANES, 1997, 1325 (01) :63-70
[7]   HySP26 gene transcription is strongly induced during Saccharomyces cerevisiae growth at low pH [J].
Carmelo, V ;
SaCorreia, I .
FEMS MICROBIOLOGY LETTERS, 1997, 149 (01) :85-88
[8]   Toxicity of linoleic acid hydroperoxide to Saccharomyces cerevisiae:: Involvement of a respiration-related process for maximal sensitivity and adaptive response [J].
Evans, MV ;
Turton, HE ;
Grant, CM ;
Dawes, IW .
JOURNAL OF BACTERIOLOGY, 1998, 180 (03) :483-490
[9]   Stationary-phase regulation of the Saccharomyces cerevisiae SOD2 gene is dependent on additive effects of HAP2/3/4/5- and STRE-binding elements [J].
FlatteryOBrien, JA ;
Grant, CM ;
Dawes, IW .
MOLECULAR MICROBIOLOGY, 1997, 23 (02) :303-312
[10]  
FLOHE L, 1984, METHOD ENZYMOL, V105, P93