Protein Synthesis during Programmed (Physiological) Cell Death

1991 ◽  
pp. 451-459
Author(s):  
R. A. Lockshin ◽  
Z. F. Zakeri ◽  
L. M. Yesner
Keyword(s):  
Cell Death ◽  
Protein Synthesis ◽  
Physiological Cell Death

scholarly journals Hypoxic neuronal necrosis: Protein synthesis-independent activation of a cell death program

2003 ◽  
Vol 100 (5) ◽  
pp. 2825-2830 ◽  
Author(s):  
J. Niquet ◽  
R. A. Baldwin ◽  
S. G. Allen ◽  
D. G. Fujikawa ◽  
C. G. Wasterlain
Keyword(s):  
Cell Death ◽  
Protein Synthesis ◽  
Neuronal Necrosis ◽  
Cell Death Program ◽  
A Cell

scholarly journals Protein synthesis persists during necrotic cell death

2005 ◽  
Vol 168 (4) ◽  
pp. 545-551 ◽  
Author(s):  
Xavier Saelens ◽  
Nele Festjens ◽  
Eef Parthoens ◽  
Isabel Vanoverberghe ◽  
Michael Kalai ◽  
...  
Keyword(s):  
Cell Death ◽  
Protein Synthesis ◽  
De Novo ◽  
Translation Initiation Factor ◽  
Initiation Factor ◽  
Necrotic Cell Death ◽  
Necrotic Cell ◽  
Proteolytic Activation ◽  
Double Stranded Rna ◽  
Molecular Events

Cell death is an intrinsic part of metazoan development and mammalian immune regulation. Whereas the molecular events orchestrating apoptosis have been characterized extensively, little is known about the biochemistry of necrotic cell death. Here, we show that, in contrast to apoptosis, the induction of necrosis does not lead to the shut down of protein synthesis. The rapid drop in protein synthesis observed in apoptosis correlates with caspase-dependent breakdown of eukaryotic translation initiation factor (eIF) 4G, activation of the double-stranded RNA-activated protein kinase PKR, and phosphorylation of its substrate eIF2-α. In necrosis induced by tumor necrosis factor, double-stranded RNA, or viral infection, de novo protein synthesis persists and 28S ribosomal RNA fragmentation, eIF2-α phosphorylation, and proteolytic activation of PKR are absent. Collectively, these results show that, in contrast to apoptotic cells, necrotic dying cells retain the opportunity to synthesize proteins.

scholarly journals Nerve growth factor withdrawal-induced cell death in neuronal PC12 cells resembles that in sympathetic neurons.

1992 ◽  
Vol 119 (6) ◽  
pp. 1669-1680 ◽  
Author(s):  
P W Mesner ◽  
T R Winters ◽  
S H Green
Keyword(s):  
Cell Death ◽  
Protein Synthesis ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Programmed Cell Death ◽  
Pc12 Cells ◽  
Sympathetic Neurons ◽  
Nerve Growth ◽  
Neuronal Pc12 Cells ◽  
New Protein

Previous studies have shown that in neuronal cells the developmental phenomenon of programmed cell death is an active process, requiring synthesis of both RNA and protein. This presumably reflects a requirement for novel gene products to effect cell death. It is shown here that the death of nerve growth factor-deprived neuronal PC12 cells occurs at the same rate as that of rat sympathetic neurons and, like rat sympathetic neurons, involves new transcription and translation. In nerve growth factor-deprived neuronal PC12 cells, a decline in metabolic activity, assessed by uptake of [3H]2-deoxyglucose, precedes the decline in cell number, assessed by counts of trypan blue-excluding cells. Both declines are prevented by actinomycin D and anisomycin. In contrast, the death of nonneuronal (chromaffin-like) PC12 cells is not inhibited by transcription or translation inhibitors and thus does not require new protein synthesis. DNA fragmentation by internucleosomal cleavage does not appear to be a consistent or significant aspect of cell death in sympathetic neurons, neuronal PC12 cells, or nonneuronal PC12 cells, notwithstanding that the putative nuclease inhibitor aurintricarboxylic acid protects sympathetic neurons, as well as neuronal and nonneuronal PC12 cells, from death induced by trophic factor removal. Both phenotypic classes of PC12 cells respond to aurintricarboxylic acid with similar dose-response characteristics. Our results indicate that programmed cell death in neuronal PC12 cells, but not in nonneuronal PC12 cells, resembles programmed cell death in sympathetic neurons in significant mechanistic aspects: time course, role of new protein synthesis, and lack of a significant degree of DNA fragmentation.

scholarly journals Bacterial Ribonuclease MazF-Mediated Apoptosis as Potential Cancer Therapy

2021 ◽  
Author(s):  
Maryam Saffarian Abbas Zadeh ◽  
Rebecca Anne MacPherson ◽  
Guohui Huang ◽  
Hui Ding ◽  
Rhonda Reigers Powell ◽  
...  
Keyword(s):  
Cell Death ◽  
Protein Synthesis ◽  
Cell Lines ◽  
Mrna Translation ◽  
Protein Translation ◽  
Programmed Death ◽  
Inhibition Of Protein Synthesis ◽  
Cancer Agent ◽  
Cell Suicide ◽  
The Impact

Abstract Programmed cell death is a dynamic and critical mechanism of cell suicide in eukaryotes and prokaryotes. MazF is a ribonuclease protein involved in bacterial intracellular programmed death. This protein cleaves mRNAs at ACA sequences, leading to inhibition of protein synthesis and triggering cell death. Given that cancer is heterogenic and has varied susceptibility to treatment, we examined the impact of MazF proteins on the growth and viability of three cancer cell lines: MCF7, HT29, and AGS. These cell lines were transfected with ACA-less mazF mRNAs and evaluated for MazF-mediated cell death. The data illustrated that efficient MazF translation leads to a significant reduction in cell viability and is modulated by structural elements of ACA-less mazF mRNAs. In the presence of MazF, the levels of activated caspase-3 and -7 were significantly elevated in transfected cells, confirming the occurrence of apoptosis. We also quantified mRNA translation on a single-cell basis in MCF7 and AGS cell lines to examine MazF-mediated inhibition of protein synthesis. MazF expression significant decreases the levels of protein translation in the examined cell lines. This is the first report of MazF as a potential anti-cancer agent via induction of apoptosis in MCF7, AGS, and HT-29 cell lines.

scholarly journals Cathepsin D gene expression outlines the areas of physiological cell death during embryonic development

2007 ◽  
Vol 236 (3) ◽  
pp. 880-885 ◽  
Author(s):  
V. Zuzarte-Luis ◽  
J.A. Montero ◽  
N. Torre-Perez ◽  
J.A. Garcia-Porrero ◽  
J.M. Hurle
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Embryonic Development ◽  
Cathepsin D ◽  
Physiological Cell Death

scholarly journals Eagle Effect in Nonreplicating Persister Mycobacteria

2015 ◽  
Vol 59 (12) ◽  
pp. 7786-7789 ◽  
Author(s):  
Mu-Lu Wu ◽  
Jasmie Tan ◽  
Thomas Dick
Keyword(s):  
Cell Death ◽  
Protein Synthesis ◽  
Dose Response ◽  
Mycobacterium Smegmatis ◽  
Content Type ◽  
Cell Death Pathway ◽  
Low Concentrations ◽  
Eagle Effect ◽  
Dependent Cell ◽  
Gyrase Inhibitors

ABSTRACTWe determined the microbicidal activities of antibacterials against nonreplicatingMycobacterium smegmatisgrown in a starvation-based Loebel model for persistence. Whereas most drugs lost their activity, fluoroquinolones retained lethal potency. Dose-response characterizations showed a paradoxical more-drug-kills-less Eagle effect. Pretreatment of cultures with chloramphenicol blocked the lethal action of the gyrase inhibitors. These results suggest that fluoroquinolones at low concentrations trigger a protein synthesis-dependent cell death pathway and shut off this suicide pathway at elevated concentrations.

Metabolic events during programmed cell death in insect labial glands

1994 ◽  
Vol 72 (11-12) ◽  
pp. 597-601 ◽  
Author(s):  
Reginald Halaby ◽  
Zahra Zakeri ◽  
Richard A. Lockshin
Keyword(s):  
Cell Death ◽  
Protein Synthesis ◽  
Acid Phosphatase ◽  
Programmed Cell Death ◽  
Manduca Sexta ◽  
Adenosine Triphosphate ◽  
Mitochondrial Respiration ◽  
Second Messengers ◽  
Labial Gland ◽  
Dying Cells

The labial gland of Manduca sexta is a valuable system to study the mechanisms of programmed cell death since the death of the gland is nearly synchronous and, except for the anterior duct, involves all of the tissue. The gland degenerates in 5 days during pupation. Our previous work documents a drop in total protein synthesis as the gland degenerates. To evaluate potential causes of this altered protein synthesis, we monitored several parameters of metabolism in dying cells: levels of adenosine triphosphate to estimate the energy resources of the gland; reduction of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide to assess mitochondrial respiration; levels of acid phosphatase to assay lysosomal enzyme activity; and concentrations of cyclic nucleotides and inositol triphosphate to monitor signaling. While protein synthesis fell precipitously on day 0, total adenosine triphosphate and mitochondrial respiration were unchanged until the cells underwent massive collapse on day 3. Lysosomal acid phosphatase increased during early metamorphosis, and ultimately the bulk of the cytoplasm was destroyed in autophagic vacuoles. Changes in the concentrations of second messengers were modest and late. The relationships between the metabolism and the collapse of the labial gland are under investigation.Key words: programmed cell death, Manduca sexta, energetics, lysosomes, second messengers, protein synthesis.

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