scholarly journals Normal development, oncogenesis and programmed cell death

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


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.


2002 ◽  
Vol 8 (5) ◽  
pp. 375-391 ◽  
Author(s):  
Michiko Watanabe ◽  
Midori Hitomi ◽  
Kathy van der Wee ◽  
Florence Rothenberg ◽  
Steven A. Fisher ◽  
...  

Programmed cell death or apoptosis occurs in many tissues during normal development and in the normal homeostasis of adult tissues. Apoptosis also plays a significant role in abnormal development and disease. Increased interest in apoptosis and cell death in general has resulted in the development of new techniques and the revival of old ones. Each assay has its advantages and disadvantages that can render it appropriate and useful for one application, but inappropriate or difficult to use in another. Understanding the strengths and limitations of the assays would allow investigators to select the best methods for their needs.


Author(s):  
Dylan J. Guerin ◽  
Cindy X. Kha ◽  
Kelly Ai-Sun Tseng

The ability to regrow lost or damaged tissues is widespread, but highly variable among animals. Understanding this variation remains a challenge in regeneration biology. Numerous studies from Hydra to mouse have shown that apoptosis acts as a potent and necessary mechanism in regeneration. Much is known about the involvement of apoptosis during normal development in regulating the number and type of cells in the body. In the context of regeneration, apoptosis also regulates cell number and proliferation in tissue remodeling. Apoptosis acts both early in the process to stimulate regeneration and later to regulate regenerative patterning. Multiple studies indicate that apoptosis acts as a signal to stimulate proliferation within the regenerative tissues, producing the cells needed for full regeneration. The conservation of apoptosis as a regenerative mechanism demonstrated across species highlights its importance and motivates the continued investigation of this important facet of programmed cell death. This review summarizes what is known about the roles of apoptosis during regeneration, and compares regenerative apoptosis with the mechanisms and function of apoptosis in development. Defining the complexity of regenerative apoptosis will contribute to new knowledge and perspectives for understanding mechanisms of apoptosis induction and regulation.


Development ◽  
2001 ◽  
Vol 128 (23) ◽  
pp. 4891-4898
Author(s):  
Stefanie Seipp ◽  
Jürgen Schmich ◽  
Thomas Leitz

Programmed cell death is not only known as a mechanism mediating tissue destruction, but also as an organismic tool for body shaping and regulation of morphological events during development. Here we report the tight and vital link of the most prominent form of programmed cell death, apoptosis, to one of the oldest, most basic, and most radical developmental processes, the metamorphosis of the marine hydrozoon Hydractinia echinata. Apoptosis, represented by DNA fragmentation, appears very early during metamorphosis, approximately 20 minutes post induction. It is then executed in a very distinct spatial and temporal pattern, including the removal or phagocytosis of a large number of larval cells prior to the appearance of stolons and tentacles. Our data indicate a developmental program striving to reduce all body parts that are no longer necessary, before reaching a distinct turning point, when the development of adult features is initiated. During these events, morphogenesis of basal and apical structures correlates with recycling of that particular larval region, indicated by the presence of apoptosis. Based on these data, the necessity of apoptosis for normal development of adult patterns is inferred and a fundamental association of apoptosis with developmental processes can be stated.


eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Cristina Aguirre-Chen ◽  
Christopher M Hammell

CED-3, a protein that is essential for programmed cell death, also has an unexpected role in the regulation of non-apoptotic genes during normal development.


2018 ◽  
Vol 34 (1) ◽  
pp. 311-332 ◽  
Author(s):  
Swapna A. Gudipaty ◽  
Christopher M. Conner ◽  
Jody Rosenblatt ◽  
Denise J. Montell

Balancing cell death and survival is essential for normal development and homeostasis and for preventing diseases, especially cancer. Conventional cell death pathways include apoptosis, a form of programmed cell death controlled by a well-defined biochemical pathway, and necrosis, the lysis of acutely injured cells. New types of regulated cell death include necroptosis, pyroptosis, ferroptosis, phagoptosis, and entosis. Autophagy can promote survival or can cause death. Newly described processes of anastasis and resuscitation show that, remarkably, cells can recover from the brink of apoptosis or necroptosis. Important new work shows that epithelia achieve homeostasis by extruding excess cells, which then die by anoikis due to loss of survival signals. This mechanically regulated process both maintains barrier function as cells die and matches rates of proliferation and death. In this review, we describe these unconventional ways in which cells have evolved to die or survive, as well as the contributions that these processes make to homeostasis and cancer.


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