scholarly journals Mitochondria-Mediated Programmed Cell Death in Saccharomyces cerevisiae Induced by Betulinic Acid Is Accelerated by the Deletion of PEP4 Gene

2019 ◽  
Vol 7 (11) ◽  
pp. 538
Author(s):  
Lu ◽  
Shu ◽  
Lou ◽  
Chen
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Animal Model ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Betulinic Acid ◽  
Pivotal Role ◽  
Induce Cell Death ◽  
Pep4 Gene ◽  
Complicated Mechanism

In this work, using Saccharomyces cerevisiae as a model, we showed that BetA could inhibitcell proliferation and lead to lethal cytotoxicity accompanying programmed cell death (PCD).Interestingly, it was found that vacuolar protease Pep4p played a pivotal role in BetA‐induced S.cerevisiae PCD. The presence of Pep4p reduced the damage of BetA‐induced cells. This work impliedthat BetA may induce cell death of S. cerevisiae through mitochondria‐mediated PCD, and thedeletion of Pep4 gene possibly accelerated the effect of PCD. The present investigation provided thepreliminary research for the complicated mechanism of BetA‐induced cell PCD regulated by vacularprotease Pep4p and lay the foundation for understanding of the Pep4p protein in an animal model.

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.

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 HCAR Is a Limitation Factor for Chlorophyll Cycle and Chlorophyll b Degradation in Chlorophyll-b-Overproducing Plants

Biomolecules ◽  
2020 ◽  
Vol 10 (12) ◽  
pp. 1639
Author(s):  
Xuan Zhao ◽  
Ting Jia ◽  
Xueyun Hu
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Metabolic Pathway ◽  
Pivotal Role ◽  
Limiting Factor ◽  
Chlorophyll B ◽  
Green Color ◽  
Chl A ◽  
Cycle Regulation

The chlorophyll (Chl) cycle is the metabolic pathway for Chl a and Chl b inter-conversion. In this pathway, Chl b is synthesized from Chl a by the catalyzing action of chlorophyllide a oxygenase (CAO). In contrast, Chl b is firstly reduced to produce 7-hydroxymethyl Chl (HMChl) a, which is catalyzed by two isozymes of Chl b reductase (CBR), non-yellow coloring 1 (NYC1) and NYC1-like (NOL). Subsequently, HMChl a is reduced to Chl a by HMChl a reductase (HCAR). CAO plays a pivotal role in Chl a/b ratio regulation and plants over-accumulate Chl b in CAO-overexpressing plants. NYC1 is more accumulated in Chl-b-overproducing plants, while HCAR is not changed. To investigate the role of HCAR in Chl cycle regulation, the Chl metabolites of Chl-b-overproducing plants were analyzed. The results showed that HMChl a accumulated in these plants, and it decreased and the Chl a/b ratio increased by overexpressing HCAR, implying HCAR is insufficient for Chl cycle in Chl-b-overproducing plants. Furthermore, during dark-induced senescence, the non-programmed cell death symptoms (leaves dehydrated with green color retained) of Chl-b-overproducing plants were obviously alleviated, and the content of HM pheophorbide (HMPheide) a and Pheide b were sharply decreased by overexpressing HCAR. These results imply that HCAR is also insufficient for Chl degradation in Chl-b-overproducing plants during senescence, thus causing the accumulation of Chl metabolites and non-programmed cell death of leaves. With these results taken together, we conclude that HCAR is not well regulated and it is a limiting factor for Chl cycle and Chl b degradation in Chl-b-overproducing plants.

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

Gene ◽  
2005 ◽  
Vol 354 ◽  
pp. 93-98 ◽  
Author(s):  
Sergio Giannattasio ◽  
Nicoletta Guaragnella ◽  
Manuela Corte-Real ◽  
Salvatore Passarella ◽  
Ersilia Marra
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Death ◽  
Acetic Acid ◽  
Programmed Cell Death ◽  
Acid Stress ◽  
Stress Adaptation

scholarly journals Deletion of Atg22 gene contributes to reduce programmed cell death induced by acetic acid stress in Saccharomyces cerevisiae

2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Jingjin Hu ◽  
Yachen Dong ◽  
Wei Wang ◽  
Wei Zhang ◽  
Hanghang Lou ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Amino Acids ◽  
Cell Death ◽  
Cell Wall ◽  
Acetic Acid ◽  
Programmed Cell Death ◽  
Cell Wall Integrity ◽  
Yeast Cells ◽  
Death Process ◽  
Lignocellulosic Biofuel

Abstract Background Programmed cell death (PCD) induced by acetic acid, the main by-product released during cellulosic hydrolysis, cast a cloud over lignocellulosic biofuel fermented by Saccharomyces cerevisiae and became a burning problem. Atg22p, an ignored integral membrane protein located in vacuole belongs to autophagy-related genes family; prior study recently reported that it is required for autophagic degradation and efflux of amino acids from vacuole to cytoplasm. It may alleviate the intracellular starvation of nutrition caused by Ac and increase cell tolerance. Therefore, we investigate the role of atg22 in cell death process induced by Ac in which attempt is made to discover new perspectives for better understanding of the mechanisms behind tolerance and more robust industrial strain construction. Results In this study, we compared cell growth, physiological changes in the absence and presence of Atg22p under Ac exposure conditions. It is observed that disruption and overexpression of Atg22p delays and enhances acetic acid-induced PCD, respectively. The deletion of Atg22p in S. cerevisiae maintains cell wall integrity, and protects cytomembrane integrity, fluidity and permeability upon Ac stress by changing cytomembrane phospholipids, sterols and fatty acids. More interestingly, atg22 deletion increases intracellular amino acids to aid yeast cells for tackling amino acid starvation and intracellular acidification. Further, atg22 deletion upregulates series of stress response genes expression such as heat shock protein family, cell wall integrity and autophagy. Conclusions The findings show that Atg22p possessed the new function related to cell resistance to Ac. This may help us have a deeper understanding of PCD induced by Ac and provide a new strategy to improve Ac resistance in designing industrial yeast strains for bioethanol production during lignocellulosic biofuel fermentation.

scholarly journals Induction of apoptosis in Saccharomyces cerevisiae results in the spontaneous maturation of tetravirus procapsids in vivo

2007 ◽  
Vol 88 (5) ◽  
pp. 1576-1582 ◽  
Author(s):  
Michele Tomasicchio ◽  
Philip Arno Venter ◽  
Karl H. J. Gordon ◽  
Terry N. Hanzlik ◽  
Rosemary Ann Dorrington
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Conformational Changes ◽  
Yeast Cells ◽  
Genomic Rnas ◽  
Virus Like Particle ◽  
Induced Apoptosis

The Tetraviridae are a family of small, non-enveloped, insect RNA viruses consisting of one or two single-stranded, positive-sense genomic RNAs encapsidated in an icosahedral capsid with T=4 symmetry. Tetravirus procapsids undergo maturation when exposed to a low pH environment in vitro. While the structural biology of the conformational changes that mediate acid-dependent maturation is well understood, little is known about the significance of acid-dependent maturation in vivo. To address this question, the capsid-coding sequence of the tetravirus Helicoverpa armigera stunt virus was expressed in Saccharomyces cerevisiae cells. Virus-like particles were shown to assemble as procapsids that matured spontaneously in vivo as the cells began to age. Growth in the presence of hydrogen peroxide or acetic acid, which induced apoptosis or programmed cell death in the yeast cells, resulted in virus-like particle maturation. The results demonstrate that assembly-dependent maturation of tetravirus procapsids in vivo is linked to the onset of apoptosis in yeast cells. We propose that the reduction in pH required for tetraviral maturation may be the result of cytosolic acidification, which is associated with the early onset of programmed cell death in infected cells.

scholarly journals Physiological regulation of yeast cell death in multicellular colonies is triggered by ammonia

2005 ◽  
Vol 169 (5) ◽  
pp. 711-717 ◽  
Author(s):  
Libuše Váchová ◽  
Zdena Palková
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Death ◽  
Transcription Factor ◽  
Programmed Cell Death ◽  
Yeast Cell ◽  
Metabolic Changes ◽  
Physiological Regulation ◽  
Unicellular Organisms ◽  
Apoptosis Inducing Factor

The existence of programmed cell death (PCD) in yeast and its significance to simple unicellular organisms is still questioned. However, such doubts usually do not reflect the fact that microorganisms in nature exist predominantly within structured, multicellular communities capable of differentiation, in which a profit of individual cells is subordinated to a profit of populations. In this study, we show that some PCD features naturally appear during the development of multicellular Saccharomyces cerevisiae colonies. An ammonia signal emitted by aging colonies triggers metabolic changes that localize yeast death only in the colony center. The remaining population can exploit the released nutrients and survives. In colonies defective in Sok2p transcription factor that are unable to produce ammonia (Váchová, L., F. Devaux, H. Kucerova, M. Ricicova, C. Jacq, and Z. Palková. 2004. J. Biol. Chem. 279:37973–37981), death is spread throughout the whole population, thus decreasing the lifetime of the colony. The absence of Mca1p metacaspase or Aif1p orthologue of mammalian apoptosis-inducing factor does not prevent regulated death in yeast colonies.

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