scholarly journals The Interplay of Key Phospholipid Biosynthetic Enzymes and the Yeast V-ATPase Pump and their Role in Programmed Cell Death

2021 ◽  
Author(s):  
Goldie Libby Sherr ◽  
Chang-Hui Shen
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Adaptive Response ◽  
Mammalian Cells ◽  
Biosynthetic Genes ◽  
Yeast Saccharomyces Cerevisiae ◽  
Growth Physiology ◽  
Vacuolar Acidification ◽  
Main Regulator

Exposure of the yeast Saccharomyces cerevisiae to environmental stress can influence cell growth, physiology and differentiation, and thus result in a cell’s adaptive response. During the course of an adaptive response, the yeast vacuoles play an important role in protecting cells from stress. Vacuoles are dynamic organelles that are similar to lysosomes in mammalian cells. The defect of a lysosome’s function may cause various genetic and neurodegenerative diseases. The multi-subunit V-ATPase is the main regulator for vacuolar function and its activity plays a significant role in maintaining pH homeostasis. The V-ATPase is an ATP-driven proton pump which is required for vacuolar acidification. It has also been demonstrated that phospholipid biosynthetic genes might influence vacuolar morphology and function. However, the mechanistic link between phospholipid biosynthetic genes and vacuolar function has not been established. Recent studies have demonstrated that there is a regulatory role of Pah1p, a phospholipid biosynthetic gene, in V-ATPase disassembly and activity. Therefore, in this chapter we will use Saccharomyces cerevisiae as a model to discuss how Pah1p affects V-ATPase disassembly and activity and how Pah1p negatively affect vacuolar function. Furthermore, we propose a hypothesis to describe how Pah1p influences vacuolar function and programmed cell death through the regulation of V-ATPase.

Nma111p, the pro-apoptotic HtrA-like nuclear serine protease in Saccharomyces cerevisiae: a short survey

2011 ◽  
Vol 39 (5) ◽  
pp. 1499-1501 ◽  
Author(s):  
Birthe Fahrenkrog
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Serine Protease ◽  
Current Knowledge ◽  
Regulatory Proteins ◽  
Dependent Manner ◽  
Yeast Saccharomyces Cerevisiae ◽  
Apoptosis Protein ◽  
Evolutionarily Conserved

The baker's yeast, Saccharomyces cerevisiae, is also capable of undergoing programmed cell death or apoptosis, for example in response to viral infection as well as during chronological and replicative aging. Intrinsically, programmed cell death in yeast can be induced by, for example, H2O2, acetic acid or the mating-type pheromone. A number of evolutionarily conserved apoptosis-regulatory proteins have been identified in yeast, one of which is the HtrA (high-temperature requirement A)-like serine protease Nma111p (Nma is nuclear mediator of apoptosis). Nma111p is a nuclear serine protease of the HtrA family, which targets Bir1p, the only known inhibitor-of-apoptosis protein in yeast. Nma111p mediates apoptosis in a serine-protease-dependent manner and exhibits its activity exclusively in the nucleus. How the activity of Nma111p is regulated has remained largely elusive, but some evidence points to a control by phosphorylation. Current knowledge of Nma111p's function in apoptosis will be discussed in the present review.

scholarly journals Translation machinery reprogramming in programmed cell death in Saccharomyces cerevisiae

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Francesco Monticolo ◽  
Emanuela Palomba ◽  
Maria Luisa Chiusano
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Death ◽  
Acetic Acid ◽  
Programmed Cell Death ◽  
Differential Expression ◽  
Ribosomal Proteins ◽  
Relative Proportion ◽  
Duplication Event ◽  
Genome Duplication Event ◽  
Cell Death Pathway

AbstractProgrammed cell death involves complex molecular pathways in both eukaryotes and prokaryotes. In Escherichia coli, the toxin–antitoxin system (TA-system) has been described as a programmed cell death pathway in which mRNA and ribosome organizations are modified, favoring the production of specific death-related proteins, but also of a minor portion of survival proteins, determining the destiny of the cell population. In the eukaryote Saccharomyces cerevisiae, the ribosome was shown to change its stoichiometry in terms of ribosomal protein content during stress response, affecting the relative proportion between ohnologs, i.e., the couple of paralogs derived by a whole genome duplication event. Here, we confirm the differential expression of ribosomal proteins in yeast also during programmed cell death induced by acetic acid, and we highlight that also in this case pairs of ohnologs are involved. We also show that there are different trends in cytosolic and mitochondrial ribosomal proteins gene expression during the process. Moreover, we show that the exposure to acetic acid induces the differential expression of further genes coding for products related to translation processes and to rRNA post-transcriptional maturation, involving mRNA decapping, affecting translation accuracy, and snoRNA synthesis. Our results suggest that the reprogramming of the overall translation apparatus, including the cytosolic ribosome reorganization, are relevant events in yeast programmed cell death induced by acetic acid.

Alpha-ketoglutarate enhances freeze–thaw tolerance and prevents carbohydrate-induced cell death of the yeast Saccharomyces cerevisiae

2017 ◽  
Vol 200 (1) ◽  
pp. 33-46 ◽  
Author(s):  
Maria M. Bayliak ◽  
Olha V. Hrynkiv ◽  
Roksolana V. Knyhynytska ◽  
Volodymyr I. Lushchak
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Death ◽  
Yeast Saccharomyces Cerevisiae ◽  
Freeze Thaw

Cytochrome c Trp65Ser substitution results in inhibition of acetic acid-induced programmed cell death in Saccharomyces cerevisiae

Mitochondrion ◽  
2011 ◽  
Vol 11 (6) ◽  
pp. 987-991 ◽  
Author(s):  
Nicoletta Guaragnella ◽  
Salvatore Passarella ◽  
Ersilia Marra ◽  
Sergio Giannattasio
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Death ◽  
Acetic Acid ◽  
Cytochrome C ◽  
Programmed Cell Death

scholarly journals Conservation of transcriptional activation functions of the NF-kappa B p50 and p65 subunits in mammalian cells and Saccharomyces cerevisiae.

1993 ◽  
Vol 13 (3) ◽  
pp. 1666-1674 ◽  
Author(s):  
P A Moore ◽  
S M Ruben ◽  
C A Rosen
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Transcriptional Activation ◽  
Mammalian Cells ◽  
Transcriptional Activity ◽  
Transcriptional Activator ◽  
Genetic System ◽  
Nf Kappa B ◽  
Yeast Saccharomyces Cerevisiae ◽  
Activation Domains ◽  
Inhibitory Molecule

The NF-kappa B transcription factor complex is composed of a 50-kDa (p50) and a 65-kDa (p65) subunit. Both subunits bind to similar DNA motifs and elicit transcriptional activation as either homo- or heterodimers. By using chimeric proteins that contain the DNA binding domain of the yeast transcriptional activator GAL4 and subdomains of p65, three distinct transcriptional activation domains were identified. One domain was localized to a region of 42 amino acids containing a potential leucin zipper structure, consistent with earlier reports. Two other domains, both acidic and rich in prolines, were also identified. Of perhaps more significance, the same minimal activation domains that were functional in mammalian cells were also functional in the yeast Saccharomyces cerevisiae. Coexpression of the NF-kappa B inhibitory molecule, I kappa B, reduced the transcriptional activity of p65 significantly, suggesting the ability of I kappa B to function in a similar manner in S. cerevisiae. Surprisingly, while the conserved rel homology domain of p65 demonstrated no transcriptional activity in either mammalian cells or S. cerevisiae, the corresponding domain in p50 was a strong transcriptional activator in S. cerevisiae. The observation that similar domains elicit transcriptional activation in mammalian cells and S. cerevisiae demonstrates strong conservation of the transcriptional machinery required for NF-kappa B function and provides a powerful genetic system to study the transcriptional mechanisms of these proteins.

scholarly journals T-2 mycotoxin induced apoptosis in broiler’s liver tissue

2018 ◽  
Vol 27 (1) ◽  
pp. 9-16
Author(s):  
Piret Hussar ◽  
Tõnu Järveots ◽  
Lazo Pendovski ◽  
Katerina Blagoevska ◽  
Trpe Ristoski ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Liver Tissue ◽  
Immunohistochemical Staining ◽  
Mammalian Cells ◽  
Gallus Domesticus ◽  
Gallus Gallus Domesticus ◽  
Histopathological Changes ◽  
Induced Apoptosis ◽  
Multicellular Organisms

Apoptosis is a process of programmed cell death that occurs in multicellular organisms. As T-2 toxin is known to induce apoptosis in mammalian cells, the aim of the present experiment was to study the toxic effect of T-2 on chicken liver tissue using apoptosis-related antibodies p21 and p53 which are involved in the p53/p21-mediated apoptotic signalling pathway. The experiment was conducted on fourteen 40-day-old broilers (Gallus gallus domesticus) who were divided into control and T-2 toxin groups. For the T-2 toxin group, T-2 toxin (Sigma, Germany) was dissolved in water and given per os for three consecutive days. The material of the liver was taken 24 hours after the last application. The specimens were fixed with 10% formalin and embedded into paraffin; slices 5 μm in thickness were cut followed by immunohistochemical staining with polyclonal primary antibodies p21 and p53 (Abcam, UK) according to the manufacturer’s guidelines (IHC kit, Abcam, UK). Strong expression of p21 and p53 found in hepatocytes, endotheliocytes and around blood vessels together with large tissue destructions in T-2 toxin group birds’ liver indicates apoptosis and histopathological changes in liver tissue during T-2 mycotoxicosis.

Mitochondrial dynamics in yeast cell death and aging

2011 ◽  
Vol 39 (5) ◽  
pp. 1520-1526 ◽  
Author(s):  
Ralf J. Braun ◽  
Benedikt Westermann
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Mitochondrial Dynamics ◽  
Progressive Increase ◽  
Mitochondrial Morphology ◽  
Aging Research ◽  
Yeast Saccharomyces Cerevisiae ◽  
Cell Death Pathways ◽  
Dependent Cell ◽  
Mitochondrial Networks

Mitochondria play crucial roles in programmed cell death and aging. Different stimuli activate distinct mitochondrion-dependent cell death pathways, and aging is associated with a progressive increase in mitochondrial damage, culminating in oxidative stress and cellular dysfunction. Mitochondria are highly dynamic organelles that constantly fuse and divide, forming either interconnected mitochondrial networks or separated fragmented mitochondria. These processes are believed to provide a mitochondrial quality control system and enable an effective adaptation of the mitochondrial compartment to the metabolic needs of the cell. The baker's yeast, Saccharomyces cerevisiae, is an established model for programmed cell death and aging research. The present review summarizes how mitochondrial morphology is altered on induction of cell death or on aging and how this correlates with the induction of different cell death pathways in yeast. We highlight the roles of the components of the mitochondrial fusion and fission machinery that affect and regulate cell death and aging.

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