Apoptosis – a death-inducing mechanism tightly linked with morphogenesis in Hydractina echinata (Cnidaria, Hydrozoa)

Development ◽  
2001 ◽  
Vol 128 (23) ◽  
pp. 4891-4898
Author(s):  
Stefanie Seipp ◽  
Jürgen Schmich ◽  
Thomas Leitz
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Dna Fragmentation ◽  
Temporal Pattern ◽  
Turning Point ◽  
Normal Development ◽  
Body Parts ◽  
Tissue Destruction ◽  
Developmental Processes ◽  
Developmental Program

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.

scholarly journals Have necrohormones a role in embryogenesis?

2014 ◽  
Vol 65 (1-2) ◽  
pp. 7-9 ◽  
Author(s):  
P. R. Bell
Keyword(s):  
Cell Death ◽  
Somatic Embryogenesis ◽  
Programmed Cell Death ◽  
Picea Abies ◽  
Recent Work ◽  
Normal Development ◽  
Living Cells ◽  
Embryogenic Cultures ◽  
Conflicting Evidence ◽  
Apomictic Reproduction

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.

Apoptosis in Degenerative Diseases of the Basal Ganglia

1998 ◽  
Vol 4 (4) ◽  
pp. 301-311 ◽  
Author(s):  
Robert E. Burke
Keyword(s):  
Cell Death ◽  
Basal Ganglia ◽  
Programmed Cell Death ◽  
Direct Evidence ◽  
Normal Development ◽  
Dopamine Neurons ◽  
Degenerative Diseases ◽  
Morphological Markers ◽  
Degenerative Disorders ◽  
New Hypothesis

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.

Internucleosomal DNA fragmentation and programmed cell death (apoptosis) in the interdigital tissue of the embryonic chick leg bud

1993 ◽  
Vol 106 (1) ◽  
pp. 201-208 ◽  
Author(s):  
V. Garcia-Martinez ◽  
D. Macias ◽  
Y. Ganan ◽  
J.M. Garcia-Lobo ◽  
M.V. Francia ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Dna Fragmentation ◽  
Limb Development ◽  
Light Transmission ◽  
Morphological Changes ◽  
Death Process ◽  
Chondrogenic Potential ◽  
Cell Death Process ◽  
Dying Cells

In this work we have attempted to characterize the programmed cell death process in the chick embryonic interdigital tissue. Interdigital cell death is a prominent phenomenon during limb development and has the role of sculpturing the digits. Morphological changes in the regressing interdigital tissue studied by light, transmission and scanning electron microscopy were correlated with the occurrence of internucleosomal DNA fragmentation, evaluated using agarose gels. Programming of the cell death process was also analyzed by testing the chondrogenic potential of the interdigital mesenchyme, in high density cultures. Our results reveal a progressive loss of the chondrogenic potential of the interdigital mesenchyme, detectable 36 hours before the onset of the degenerative process. Internucleosomal DNA fragmentation was only detected concomitant with the appearance of cells dying with the morphology of apoptosis, but unspecific DNA fragmentation was also present at the same time. This unspecific DNA fragmentation was explained by a precocious activation of the phagocytic removal of the dying cells, confirmed in the tissue sections. From our observations it is suggested that programming of cell death involves changes before endonuclease activation. Further, cell surface changes involved in the phagocytic uptake of the dying cells appear to be as precocious as endonuclease activation.

scholarly journals Programmed Cell Death in Human Ovary Is a Function of Follicle and Corpus Luteum Status*

1997 ◽  
Vol 82 (9) ◽  
pp. 3148-3155
Author(s):  
Wei Yuan ◽  
Linda C. Giudice
Keyword(s):  
Molecular Weight ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Corpus Luteum ◽  
Dna Fragmentation ◽  
Low Molecular Weight ◽  
Corpora Lutea ◽  
Positive Staining ◽  
Human Ovary ◽  
Dna Laddering

Abstract Although extensive investigation on follicular apoptosis (programmed cell death) has been conducted in the infraprimate ovary, there is little information regarding apoptosis and its relationship to follicular status in the human. In this study, apoptosis was investigated in 116 human ovarian follicles (primordial to dominant) and 5 corpora lutea from a total of 27 premenopausal women. Follicles and corpora lutea were evaluated for the presence of DNA fragmentation, characteristic of apoptosis, by two methods: in situ hybridization using 3′ end-labeling of DNA with digoxigenin-labeled nucleotides and subsequent digoxigenin antibody and peroxidase staining, and/or biochemical analysis of low molecular weight DNA laddering. Follicle functional status was evaluated by determining follicle sizes and follicular fluid androgen/estrogen (A/E) ratios. No apoptosis was observed in 67 primordial, primary, or secondary follicles. Positive staining for DNA fragmentation was found in a few granulosa cells in 0.1- to 2-mm follicles, whereas abundant staining in granulosa was detected in 2.1- to 9.9-mm follicles. In contrast, no DNA fragmentation was detected in dominant follicles (10–16 mm). The frequency of apoptosis in follicles was calculated to be 37% in 0.1- to 2-mm follicles, 50% in 2.1- to 5-mm follicles, and 27% in 5.1- to 9.9-mm follicles. Abundant low molecular weight DNA laddering was only found in androgen-dominant follicles and not in estrogen-dominant follicles. Positive staining for DNA fragmentation and low molecular weight DNA laddering were observed in degenerating but not healthy-appearing corpora lutea. In the former, DNA fragmentation was found primarily in large luteal cells. These data suggest that follicular atresia in human ovary results from normal programmed cell death and primarily occurs in the granulosa cell layers of the early antral and &lt;10-mm antral follicles primarily. Furthermore, because apoptosis occurs as early as the 200-mm stage, follicle selection may begin as early as the initial formation of the antrum. The results also suggest that degeneration of the corpus luteum occurs by apoptotic mechanisms.

scholarly journals Normal development, oncogenesis and programmed cell death

Oncogene ◽  
1998 ◽  
Vol 17 (10) ◽  
pp. 1189-1194 ◽  
Author(s):  
Dan A Liebermann
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Normal Development

Bcl-2 and Bax expression in adult rat hearts after coronary occlusion: age-associated differences

1998 ◽  
Vol 275 (1) ◽  
pp. R315-R322 ◽  
Author(s):  
Lixin Liu ◽  
Gohar Azhar ◽  
Wei Gao ◽  
Xiaomin Zhang ◽  
Jeanne Y. Wei
Keyword(s):  
Cell Death ◽  
Young Adult ◽  
Programmed Cell Death ◽  
Dna Fragmentation ◽  
Coronary Occlusion ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Age Related ◽  
Rat Hearts ◽  
Coronary Ligation

It has been reported that programmed cell death (apoptosis) occurs during myocardial infarction. The influence of age on programmed cell death or DNA fragmentation after coronary occlusion has not been extensively characterized. To test the hypothesis that there are age-related differences in susceptibility to DNA fragmentation during ischemia-infarction, we studied DNA fragmentation in young adult and old male F344 rat hearts after acute coronary artery occlusion. Hearts were studied at 1, 3, and 5 h and 1 and 7 days after coronary ligation. The percentage of apoptotic cells was determined by the in situ end-labeling technique, and internucleosomal fragmentation (DNA laddering) pattern was also analyzed. Our results show that 1) DNA fragmentation began earlier and peaked earlier in the old compared with young adult hearts during infarction; 2) there was heightened expression of both Bcl-2 and Bax in the old hearts at baseline; and 3) the Bcl-2-to-Bax ratio was higher in the older heart after coronary ligation. These results suggest that, compared with the young adult heart, the aged heart may be more susceptible to ischemia-induced DNA fragmentation.

Physiological programmed cell death in thymocytes is induced by physical stress (exercise)

1993 ◽  
Vol 265 (3) ◽  
pp. C626-C629 ◽  
Author(s):  
J. P. Concordet ◽  
A. Ferry
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Dna Fragmentation ◽  
Rest Period ◽  
Physical Stress ◽  
Agarose Gel Electrophoresis ◽  
Thymic Involution ◽  
Ru 486 ◽  
Cell Numbers ◽  
Male Wistar Rats

Thymic involution occurs in young adult male Wistar rats that have performed two runs to exhaustion (RTE) on a treadmill, separated by a 24-h rest period, but not after a single RTE. We were interested in determining whether programmed cell death (or apoptosis) is responsible for the corresponding decrease in T-cell numbers in the thymus. DNA fragmentation, which is an early feature of apoptosis and easily detected by agarose gel electrophoresis, was found in rat thymocytes after the second RTE (the duration of 1 RTE was approximately 5 h). It was also detected after a single RTE or after 2.5 h of running only, and the levels of DNA fragmentation were always roughly similar. In addition, DNA fragmentation was decreased in RU-486 vs. vehicle-treated rats that had run for 2.5 h. These results indicate that physical stress induces glucocorticoid receptor-mediated apoptosis of rat thymocytes. Because apoptosis is induced to similar levels during mild and severe physical stresses, some additional events must be associated to provoke thymic involution.

DNA fragmentation and caspase-independent programmed cell death by modulated electrohyperthermia

2014 ◽  
Vol 190 (9) ◽  
pp. 815-822 ◽  
Author(s):  
N. Meggyeshazi ◽  
G. Andocs ◽  
L. Balogh ◽  
P. Balla ◽  
G. Kiszner ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Dna Fragmentation
Sign in / Sign up

Export Citation Format

Share Document