Programmed cell death in the tobacco hornworm,Manduca sexta: Alteration in protein synthesis

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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Autophagic and apoptotic features during programmed cell death in the fat body of the tobacco hornworm (Manduca sexta)

European Journal of Cell Biology ◽

10.1078/0171-9335-00359 ◽

2004 ◽

Vol 83 (2) ◽

pp. 67-78 ◽

Cited By ~ 34

Author(s):

Ferenc Müller ◽

Csaba Ádori ◽

Miklós Sass

Keyword(s):

Cell Death ◽

Programmed Cell Death ◽

Manduca Sexta ◽

Fat Body ◽

Tobacco Hornworm

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Programmed cell death: early changes in metamorphosing cells

Biochemistry and Cell Biology ◽

10.1139/o94-078 ◽

1994 ◽

Vol 72 (11-12) ◽

pp. 589-596 ◽

Cited By ~ 21

Author(s):

Richard A. Lockshin ◽

Zahra Zakeri

Keyword(s):

Cell Death ◽

Protein Synthesis ◽

Programmed Cell Death ◽

Manduca Sexta ◽

Energy Resources ◽

Type Ii ◽

Heavy Load ◽

Lysosomal Compartment ◽

Active Cell Death ◽

Labial Glands

Programmed cell death in intersegmental muscles and labial glands of Manduca sexta is a type II form of active cell death, in which lysosomal destruction of cytoplasm is a prominent and early feature, and the collapse of the nucleus is late and relatively modest until the bulk of the cytoplasm has been eroded. The prominent features of this collapse include an early expansion of the lysosomal compartment and a decrease in overall protein synthesis, while a small number of mRNAs persist or are upregulated. Energy resources appear to be adequate during the early stages of degeneration, and changes in levels of second messages likewise do not seem to be sufficiently dramatic to explain the failure of the tissue. There is some suggestion that DNA may not be completely intact long before the labial gland finally collapses, suggesting that it may fail under heavy load. Otherwise, we do not yet have an explanation for the precipitous drop in overall protein synthesis.Key words: programmed cell death, apoptosis, lysosomes, endonuclease, protein synthesis, Manduca sexta.

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

The Journal of Cell Biology ◽

10.1083/jcb.119.6.1669 ◽

1992 ◽

Vol 119 (6) ◽

pp. 1669-1680 ◽

Cited By ~ 156

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.

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