Article
Catalase T and Cu,Zn-superoxide dismutase in the acetic acid-induced programmed cell death in Saccharomyces cerevisiae.
Dipartimento di Scienze per la Salute, Università del Molise, Via De Sanctis I, Campobasso, Italy.
FEBS Letters (impact factor:
3.54).
02/2008;
582(2):210-4.
DOI:10.1016/j.febslet.2007.12.007
Source: PubMed
-
Citations (0)
- Cited In (8)
-
Article: The role of mitochondria in yeast programmed cell death.
[show abstract] [hide abstract]
ABSTRACT: Mammalian apoptosis and yeast programmed cell death (PCD) share a variety of features including reactive oxygen species production, protease activity and a major role played by mitochondria. In view of this, and of the distinctive characteristics differentiating yeast and multicellular organism PCD, the mitochondrial contribution to cell death in the genetically tractable yeast Saccharomyces cerevisiae has been intensively investigated. In this mini-review we report whether and how yeast mitochondrial function and proteins belonging to oxidative phosphorylation, protein trafficking into and out of mitochondria, and mitochondrial dynamics, play a role in PCD. Since in PCD many processes take place over time, emphasis will be placed on an experimental model based on acetic acid-induced PCD (AA-PCD) which has the unique feature of having been investigated as a function of time. As will be described there are at least two AA-PCD pathways each with a multifaceted role played by mitochondrial components, in particular by cytochrome c.Frontiers in oncology. 01/2012; 2:70. -
Article: Ycf1p attenuates basal level oxidative stress response in Saccharomyces cerevisiae.
[show abstract] [hide abstract]
ABSTRACT: Ycf1p function is regulated by casein kinase 2α, Cka1p, via phosphorylation of Ser251. Cka1p-mediated phosphorylation of Ycf1p is attenuated in response to high salt stress. Previous results from our lab suggest a role for Ycf1p in cellular resistance to salt stress. Here, we show that Ycf1p plays an important role in cellular resistance to salt stress by maintaining the cellular redox balance via glutathione recycling. Our results suggest that during acute salt stress increased Sod1p, Sod2p and Ctt1p activity is the main compensatory for the loss in Ycf1p function that results from reduced Ycf1p-dependent recycling of cellular GSH levels.FEBS letters 03/2012; 586(6):847-53. · 3.54 Impact Factor -
Article: Molecular mechanisms of Saccharomyces cerevisiae stress adaptation and programmed cell death in response to acetic acid.
[show abstract] [hide abstract]
ABSTRACT: Beyond its classical biotechnological applications such as food and beverage production or as a cell factory, the yeast Saccharomyces cerevisiae is a valuable model organism to study fundamental mechanisms of cell response to stressful environmental changes. Acetic acid is a physiological product of yeast fermentation and it is a well-known food preservative due to its antimicrobial action. Acetic acid has recently been shown to cause yeast cell death and aging. Here we shall focus on the molecular mechanisms of S. cerevisiae stress adaptation and programmed cell death in response to acetic acid. We shall elaborate on the intracellular signaling pathways involved in the cross-talk of pro-survival and pro-death pathways underlying the importance of understanding fundamental aspects of yeast cell homeostasis to improve the performance of a given yeast strain in biotechnological applications.Frontiers in microbiology. 01/2013; 4:33.
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed.
The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual
current impact factor.
Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence
agreement may be applicable.
Keywords
AA
AA treatment
AA-PCD
acetic acid
C-Y
catalase activity
cell death
constant en route
CTT1-Y
enzyme activity
H2O2 levels
hydrogen peroxide
over-expressed catalase activity
Saccharomyces cerevisiae cells
SOD
SOD activity
SOD1-Y
superoxide dismutase