scholarly journals The Reaper-Binding Protein Scythe Modulates Apoptosis and Proliferation during Mammalian Development

2005 ◽  
Vol 25 (23) ◽  
pp. 10329-10337 ◽  
Author(s):  
Fabienne Desmots ◽  
Helen R. Russell ◽  
Youngsoo Lee ◽  
Kelli Boyd ◽  
Peter J. McKinnon

ABSTRACT Scythe (BAT3 [HLA-B-associated transcript 3]) is a nuclear protein that has been implicated in apoptosis, as it can modulate Reaper, a central apoptotic regulator in Drosophila melanogaster. While Scythe can markedly affect Reaper-dependent apoptosis in Xenopus laevis cell extracts, the function of Scythe in mammals is unknown. Here, we report that inactivation of Scythe in the mouse results in lethality associated with pronounced developmental defects in the lung, kidney, and brain. In all cases, these developmental defects were associated with dysregulation of apoptosis and cellular proliferation. Scythe − / − cells were also more resistant to apoptosis induced by menadione and thapsigargin. These data show that Scythe is critical for viability and normal development, probably via regulation of programmed cell death and cellular proliferation.

2014 ◽  
Vol 65 (1-2) ◽  
pp. 7-9 ◽  
Author(s):  
P. R. Bell

The recognition of apoptosis (programmed cell death) as an accompaniment of normal development, the products released by the protoplasts undergoing self-destruction being utilized by adjacent living cells, stimulates renewed interest in Haberlandt's concept of "necrohormones" playing a role in apomictic reproduction. Recent work on somatic embryogenesis in carrot shows that regular death of certain cells in embryogenic cultures satifies the criteria of apoptosis. Similar observations have been made with embryogenic cultures of <em>Picea abies</em>. Haberlandt's claim that cell death induced by injury adjacent to an ovule in <em>Oenothera</em> could lead to parthenogenesis, despite conflicting evidence from later experimenters, is worthy of reexamination.


1998 ◽  
Vol 4 (4) ◽  
pp. 301-311 ◽  
Author(s):  
Robert E. Burke

Degenerative disorders of the basal ganglia are characterized by disturbances of motor control. Prototypic examples are Parkinson's disease, which is caused by degeneration of dopamine neurons of the substantia nigra, and Huntington's disease, which is caused by degeneration of neurons of the striatum. In recent years, it has been postulated that some of these disorders may be caused by programmed cell death or apoptosis, a genetically regulated form of cell death. There is clear evidence that apoptosis occurs in neurons of the basal ganglia during normal development, that it can be regulated, and that it can be induced in some animal models of these disorders. Although there is some suggestive direct evidence that apoptosis may occur in the human brain in these disorders, the evidence to date is partial and not yet compelling. Nevertheless, programmed cell death is an important new hypothesis for the pathogenesis of these disorders and warrants vigorous further investigation, particularly with molecular markers in addition to classic morphological markers. The concept of programmed cell death is relevant not only to the pathogenesis of these diseases but also to therapeutic issues, such as transplantation approaches.


Oncogene ◽  
1998 ◽  
Vol 17 (10) ◽  
pp. 1189-1194 ◽  
Author(s):  
Dan A Liebermann

2013 ◽  
Vol 4 (3) ◽  
pp. 259-275 ◽  
Author(s):  
Michael J. Morgan ◽  
Zheng-gang Liu

AbstractProgrammed cell death is the process by which an individual cell in a multicellular organism commits cellular ‘suicide’ to provide a long-term benefit to the organism. Thus, programmed cell death is important for physiological processes such as development, cellular homeostasis, and immunity. Importantly, in this process, the cell is not eliminated in response to random events but in response to an intricate and genetically defined set of internal cellular molecular events or ‘program’. Although the apoptotic process is generally very well understood, programmed cell death that occurs with a necrotic-like phenotype has been much less studied, and it is only within the past few years that the necrotic program has begun to be elucidated. Originally, programmed necrosis was somewhat dismissed as a nonphysiological phenomenon that occurs in vitro. Recent in vivo studies, however, suggest that regulated necrosis is an authentic classification of cell death that is important in mammalian development and other physiological processes, and programmed necrosis is now considered a significant therapeutic target in major pathological processes as well. Although the RIP1-RIP3-dependent necrosome complex is recognized as being essential for the execution of many instances of programmed necrosis, other downstream and related necrotic molecules and pathways are now being characterized. One of the current challenges is understanding how and under what conditions these pathways are linked together.


2002 ◽  
Vol 9 (2) ◽  
pp. 59-69 ◽  
Author(s):  
S. Gorski ◽  
M. Marra

Programmed cell death (PCD) is an essential and wide-spread physiological process that results in the elimination of cells. Genes required to carry out this process have been identified, and many of these remain the subjects of intense investigation. Here, we describe PCD, its functions, and some of the consequences when it goes awry. We review PCD in the model system, the fruit fly, Drosophila melanogaster, with a particular emphasis on cell death gene discovery resulting from both genetics and genomics-based approaches.


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