Deletion of AIF1 but not of YCA1/MCA1 protects Saccharomyces cerevisiae and Candida albicans cells from caspofungin-induced programmed cell death

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.

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

Mitochondrion ◽

10.1016/j.mito.2011.08.007 ◽

2011 ◽

Vol 11 (6) ◽

pp. 987-991 ◽

Cited By ~ 5

Author(s):

Nicoletta Guaragnella ◽

Salvatore Passarella ◽

Ersilia Marra ◽

Sergio Giannattasio

Keyword(s):

Saccharomyces Cerevisiae ◽

Cell Death ◽

Acetic Acid ◽

Cytochrome C ◽

Programmed Cell Death

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

Gene ◽

10.1016/j.gene.2005.03.030 ◽

2005 ◽

Vol 354 ◽

pp. 93-98 ◽

Cited By ~ 73

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

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RNA-Seq-based transcriptomic and metabolomic analysis reveal stress responses and programmed cell death induced by acetic acid in Saccharomyces cerevisiae

Scientific Reports ◽

10.1038/srep42659 ◽

2017 ◽

Vol 7 (1) ◽

Cited By ~ 26

Author(s):

Yachen Dong ◽

Jingjin Hu ◽

Linlin Fan ◽

Qihe Chen

Keyword(s):

Saccharomyces Cerevisiae ◽

Cell Death ◽

Acetic Acid ◽

Programmed Cell Death ◽

Stress Responses ◽

Metabolomic Analysis ◽

Rna Seq

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

Biotechnology for Biofuels ◽

10.1186/s13068-019-1638-x ◽

2019 ◽

Vol 12 (1) ◽

Cited By ~ 2

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.

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Ras pathway signaling accelerates programmed cell death in the pathogenic fungus Candida albicans

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.0506405103 ◽

2006 ◽

Vol 103 (3) ◽

pp. 726-731 ◽

Cited By ~ 105

Author(s):

A. J. Phillips ◽

J. D. Crowe ◽

M. Ramsdale

Keyword(s):

Cell Death ◽

Candida Albicans ◽

Programmed Cell Death ◽

Pathogenic Fungus ◽

Ras Pathway

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

Journal of General Virology ◽

10.1099/vir.0.82250-0 ◽

2007 ◽

Vol 88 (5) ◽

pp. 1576-1582 ◽

Cited By ~ 17

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.

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Yeast Bax Inhibitor, Bxi1p, Is an ER-Localized Protein That Links the Unfolded Protein Response and Programmed Cell Death in Saccharomyces cerevisiae

PLoS ONE ◽

10.1371/journal.pone.0020882 ◽

2011 ◽

Vol 6 (6) ◽

pp. e20882 ◽

Cited By ~ 34

Author(s):

James Cebulski ◽

Joshua Malouin ◽

Nathan Pinches ◽

Vincent Cascio ◽

Nicanor Austriaco

Keyword(s):

Saccharomyces Cerevisiae ◽

Cell Death ◽

Programmed Cell Death ◽

Unfolded Protein Response ◽

Unfolded Protein ◽

The Unfolded Protein Response ◽

Protein Response

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

The Journal of Cell Biology ◽

10.1083/jcb.200410064 ◽

2005 ◽

Vol 169 (5) ◽

pp. 711-717 ◽

Cited By ~ 139

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

10.5772/intechopen.97886 ◽

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.

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