Programmed cell death: Dying cells synthesize a co‐ordinated, unique set of proteins in two different episodes of cell death

Wadewitz, A. G.; Lockshin, Richard A.

doi:10.1016/0014-5793(88)81022-6

Cited by 53 publications

(17 citation statements)

References 23 publications

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“…Following this essential role, declining levels of ecdysone trigger the rapid degeneration and eventual removal of the ISMs. The requirement for de novo protein synthesis in involution of the ISMs (Lockshin, 1969,Wadewitz andLockshin, 1988) has been clearly linked to transcriptional regulation through molecular cloning of both up-and down-regulated genes (Schwartz et al, 1990). Genes for actin, myosin and the 20S proteasome unit are downregulated (Schwartz et al, 1993;Jones et al, 1995), while those for polyubiquitin , the 26S proteasome units and other proteins are up-regulated at the onset of involution (Dawson et al, 1996, Kuelzer et al, 1999Sun et al, 1996;Low et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Programmed cell death in flight muscle histolysis of the house cricket

Oliver

Albury

Mousseau

2007

Journal of Insect Physiology

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We have characterized the process of flight muscle histolysis in the female house cricket, Acheta domesticus, through analysis of alterations of tissue wet weight, total protein content, and percent shortening of the dorsal longitudinal flight muscles (DLMs). Our objectives were to (1) define the normal course of histolysis in the cricket, (2) analyze the effects of juvenile hormone (JH) removal and replacement, (3) determine the effects of cycloheximide treatment, and (4) examine patterns of protein expression during histolysis.Our results suggest that flight muscle histolysis in the house cricket is an example of an active, developmentally regulated cell death program induced by an endocrine signal. Initial declines of total protein in DLMs indicated the JH signal that induced histolysis occurred by Day 2 and that histolysis was essentially complete by Day 3. Significant reductions in tissue weight and percent muscle shortening were observed in DLMs from Day 3 crickets. Cervical ligation of Day 1 crickets prevented histolysis but this inhibition could be reversed by continual topical treatments with methoprene (an active JH analog) although ligation of Day 2 crickets did not prevent histolysis. A requirement for active protein expression was demonstrated by analysis of synthesis block by cycloheximide and short-term incorporation of 35 S-methionine. Treatment with cycloheximide prevented histolysis. Autofluorographic imaging of DLM proteins separated by electrophoresis revealed apparent coordinated regulation of protein expression.

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Section: Discussionmentioning

confidence: 99%

Programmed cell death in flight muscle histolysis of the house cricket

Oliver

Albury

Mousseau

2007

Journal of Insect Physiology

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“…The regulated expression of specific "death genes" (Ellis and Horvitz, 1986;Wadewitz and Lockshin, 1988;Schwartz et al, 1990) appears to be instrumental to this process, since RNA and protein synthesis inhibitors prevent or delay the onset of cell death (Schwartz et al, 1990;Oppenheim et al, 1990). Of late, two exceptional invertebrate models, the tobacco hornworm Manduca sexta and the nematode Caenorhabditis elegans have begun to provide tremendous insight into the genetic and molecular pathways regulating cell death during development.…”

Section: Introductionmentioning

confidence: 99%

A cyclical, developmentally‐regulated death phenomenon in a colonial urochordate

Lauzon

Ishizuka

Weissman

1992

Developmental Dynamics

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Botryllus schlosseri is a colonial ascidian whose asexually derived, clonally modular systems of zooids exhibit developmental synchrony. The blastogenic cycle culminates in a phase of programmed cell and zooid death called takeover, in which all functional zooids die over a 30 hr period, and are replaced by a new generation of individuals. Because of the weekly recurrence and magnitude of visceral death in this model organism, we have begun to characterize the mechanisms that govern takeover. Here we describe a monoclonal antibody (B3F12.9) that recognizes a novel 57 Kd polypeptide (under reducing conditions) localized to the perivisceral extracellular matrix (PVEM) of buds and zooids, as well as blood cells of Botryllus by immunofluorescence and immunogold labeling of tissue sections. During their active feeding phase, zooids exhibited a uniform labeling pattern of PVEM along their anteroposterior (A-P) axis. At the onset of takeover (T = 3 hr), B3F12.9 immunostaining became diffuse or absent at the anterior end, which paralleled the axis of contraction of the dying zooid, whereas the posterior end retained its labeling integrity. During mid (T = 15 hr) to late (T = 28 hr) takeover, issue damage was extensive, large blood macrophages and other B3F12.9 immunoreactive blood cells invaded the peribranchial cavity, whereas PVEM labeling gradually disappeared along the entire A-P axis. These findings indicate that takeover is a dynamic process in which extracellular matrix breakdown proceeds in a polarized fashion, beginning at the anterior end of each zooid and gradually propagating toward the posterior end. o 1992 WiIey-Liss, Inc.

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“…Novel RNAs and proteins are induced in regressing tissues during the period of cell death (27,42), and the expression of several constitutive gene products becomes markedly enhanced (5). The importance of synthetic activity is further shown by experiments in which either RNA or protein synthesis inhibitors can delay or prevent programmed death (37,39).…”

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confidence: 99%

Induction of the TRPM-2 gene in cells undergoing programmed death.

Buttyan¹,

Olsson²,

Pintar³

et al. 1989

Mol. Cell. Biol.

449

200

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RNA and protein products encoded by the testosterone-repressed prostate message-2 gene (TRPM-2) are induced to high levels, coordinate with the onset of cell death, in numerous rodent models of inducible tissue damage. These models include cell death initiated by hormonal stimuli (prostate regression), pressure insult (renal atrophy after ureteral obstruction), developmental stimuli (necrosis of interdigital tissue), and cytotoxic injury (chemotherapeutic regression of a tumor). Sequence analysis of cDNA encoding TRPM-2 revealed its close homology with a product referred to as SGP-2 or clusterin expressed constitutively by Sertoli cells; however, the immunologically related polypeptides expressed in regressing tissues differ in molecular mass from the forms secreted by the testis. Although the function(s) of the products encoded by the TRPM-2 gene remains unclear, their presence provides a remarkable and early indicator of programmed cell death in many types of mammalian cells.

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Programmed cell death: Dying cells synthesize a co‐ordinated, unique set of proteins in two different episodes of cell death

Cited by 53 publications

References 23 publications

Programmed cell death in flight muscle histolysis of the house cricket

Programmed cell death in flight muscle histolysis of the house cricket

A cyclical, developmentally‐regulated death phenomenon in a colonial urochordate

Induction of the TRPM-2 gene in cells undergoing programmed death.

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