scholarly journals Characterization of the endogenous deoxyribonuclease involved in nuclear DNA degradation during apoptosis (programmed cell death).

1993 ◽  
Vol 12 (1) ◽  
pp. 371-377 ◽  
Author(s):  
M.C. Peitsch ◽  
B. Polzar ◽  
H. Stephan ◽  
T. Crompton ◽  
H.R. MacDonald ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Nuclear Dna ◽  
Dna Degradation

scholarly journals Ca2+-dependent nuclease is involved in DNA degradation during the formation of the secretory cavity by programmed cell death in fruit of Citrus grandis ‘Tomentosa’

2020 ◽  
Vol 71 (16) ◽  
pp. 4812-4827 ◽  
Author(s):  
Mei Bai ◽  
Minjian Liang ◽  
Bin Huai ◽  
Han Gao ◽  
Panpan Tong ◽  
...  
Keyword(s):  
Cell Death ◽  
In Situ Hybridization ◽  
Programmed Cell Death ◽  
Nuclear Dna ◽  
Expression Patterns ◽  
Citrus Fruit ◽  
Dna Degradation ◽  
Secretory Cavity ◽  
Spatio Temporal

Abstract The secretory cavity is a typical structure in Citrus fruit and is formed by schizolysigeny. Previous reports have indicated that programmed cell death (PCD) is involved in the degradation of secretory cavity cells in the fruit, and that the spatio-temporal location of calcium is closely related to nuclear DNA degradation in this process; however, the molecular mechanisms underlying this Ca2+ regulation remain largely unknown. Here, we identified CgCaN that encodes a Ca2+-dependent DNase in the fruit of Citrus grandis ‘Tomentosa’, the function of which was studied using calcium ion localization, DNase activity assays, in situ hybridization, and protein immunolocalization. The results suggested that the full-length cDNA of CgCaN contains an ORF of 1011 bp that encodes a protein 336 amino acids in length with a SNase-like functional domain. CgCaN digests dsDNA at neutral pH in a Ca2+-dependent manner. In situ hybridization signals of CgCaN were particularly distributed in the secretory cavity cells. Ca2+ and Ca2+-dependent DNases were mainly observed in the condensed chromatin and in the nucleolus. In addition, spatio-temporal expression patterns of CgCaN and its protein coincided with the time-points that corresponded to chromatin degradation and nuclear rupture during the PCD in the development of the fruit secretory cavity. Taken together, our results suggest that Ca2+-dependent DNases play direct roles in nuclear DNA degradation during the PCD of secretory cavity cells during Citrus fruit development. Given the consistency of the expression patterns of genes regulated by calmodulin (CaM) and calcium-dependent protein kinases (CDPK) and the dynamics of calcium accumulation, we speculate that CaM and CDPK proteins might be involved in Ca2+ transport from the extracellular walls through the cytoplasm and into the nucleus to activate CgCaN for DNA degradation.

scholarly journals Zn2+-Dependent Nuclease Is Involved in Nuclear Degradation during the Programmed Cell Death of Secretory Cavity Formation in Citrus grandis ‘Tomentosa’ Fruits

Cells ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 3222
Author(s):  
Minjian Liang ◽  
Mei Bai ◽  
Hong Wu
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Late Stage ◽  
Nuclear Dna ◽  
Dna Degradation ◽  
Secretory Cells ◽  
Cavity Formation ◽  
Secretory Cavity ◽  
Cytochemical Localization ◽  
Nuclear Degradation

Zn2+- and Ca2+-dependent nucleases exhibit activity toward dsDNA in the four classes of cation-dependent nucleases in plants. Programmed cell death (PCD) is involved in the degradation of cells during schizolysigenous secretory cavity formation in Citrus fruits. Recently, the Ca2+-dependent DNase CgCAN was proven to play a key role in nuclear DNA degradation during the PCD of secretory cavity formation in Citrus grandis ‘Tomentosa’ fruits. However, whether Zn2+-dependent nuclease plays a role in the PCD of secretory cells remains poorly understood. Here, we identified a Zn2+-dependent nuclease gene, CgENDO1, from Citrus grandis ‘Tomentosa’, the function of which was studied using Zn2+ ions cytochemical localization, DNase activity assays, in situ hybridization, and protein immunolocalization. The full-length cDNA of CgENDO1 contains an open reading frame of 906 bp that encodes a protein 301 amino acids in length with a S1/P1-like functional domain. CgENDO1 degrades linear double-stranded DNA at acidic and neutral pH. CgENDO1 is mainly expressed in the late stage of nuclear degradation of secretory cells. Further spatiotemporal expression patterns of CgENDO1 showed that CgENDO1 is initially located on the endoplasmic reticulum and then moves into intracellular vesicles and nuclei. During the late stage of nuclear degradation, it was concentrated in the area of nuclear degradation involved in nuclear DNA degradation. Our results suggest that the Zn2+-dependent nuclease CgENDO1 plays a direct role in the late degradation stage of the nuclear DNA in the PCD of secretory cavity cells of Citrus grandis ‘Tomentosa’ fruits.

Biochemical characterization of programmed cell death in NGF-deprived sympathetic neurons

1992 ◽  
Vol 23 (9) ◽  
pp. 1205-1220 ◽  
Author(s):  
David P. Martin ◽  
Akira Ito ◽  
Kazuhiko Horigome ◽  
Patricia A. Lampe ◽  
Eugene M. Johnson
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Biochemical Characterization ◽  
Sympathetic Neurons

scholarly journals Mechanisms of programmed cell death

2019 ◽  
Vol 6 (4) ◽  
pp. 156-158
Author(s):  
Abdu-Alhameed A Ali Azzwali ◽  
 Azab Elsayed Azab
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Nuclear Dna ◽  
Chromatin Condensation ◽  
Cell Shrinkage ◽  
Membrane Blebbing ◽  
Development And Aging ◽  
Nuclear Dna Fragmentation ◽  
Dependent Pathway

The present review aims to spotlight on the mechanisms and stages of programmed cell death. Apoptosis, known as programmed cell death, is a homeostatic mechanism that generally occurs during development and aging in order to keep cells in tissue. It can also act as a protective mechanism, for example, in immune response or if cells are damaged by toxin agents or diseases. In cancer treatment, drugs and irradiation used in chemotherapy leads to DNA damage, which results in triggering apoptosis through the p53 dependent pathway in cancer treatment, drugs and irradiation used in chemotherapy leads to DNA damage, which results in triggering apoptosis through the p53 dependent pathway. Corticosteroids can cause apoptotic death in a number of cells. A number of changes in cell morphology are related to the different stages of apoptosis, which includes nuclear DNA fragmentation, cell shrinkage, chromatin condensation, membrane blebbing, and the formation of apoptotic bodies. There are three pathways for apoptosis, the intrinsic (mitochondrial) and extrinsic (death receptor) are the two major paths that are interlinked and that can effect one another. Conclusion: It can be concluded that apoptosis is a homeostatic mechanism that generally occurs during development and aging in order to keep cells in tissue. Drugs and irradiation used in chemotherapy leads to DNA damage, which results in triggering apoptosis through the p53 dependent pathway. The apoptosis, stages are includes nuclear DNA fragmentation, cell shrinkage, chromatin condensation, membrane blebbing, and the formation of apoptotic bodies. There are three pathways for apoptosis.

Widespread programmed cell death in proliferative and postmitotic regions of the fetal cerebral cortex

Development ◽  
1996 ◽  
Vol 122 (4) ◽  
pp. 1165-1174 ◽  
Author(s):  
A.J. Blaschke ◽  
K. Staley ◽  
J. Chun
Keyword(s):  
Cell Death ◽  
Cerebral Cortex ◽  
Programmed Cell Death ◽  
Nuclear Dna ◽  
Temporal Distribution ◽  
Embryonic Cell ◽  
Postnatal Life ◽  
Neuron Development ◽  
Cortical Cells ◽  
Dying Cells

A key event in the development of the mammalian cerebral cortex is the generation of neuronal populations during embryonic life. Previous studies have revealed many details of cortical neuron development including cell birthdates, migration patterns and lineage relationships. Programmed cell death is a potentially important mechanism that could alter the numbers and types of developing cortical cells during these early embryonic phases. While programmed cell death has been documented in other parts of the embryonic central nervous system, its operation has not been previously reported in the embryonic cortex because of the lack of cell death markers and the difficulty in following the entire population of cortical cells. Here, we have investigated the spatial and temporal distribution of dying cells in the embryonic cortex using an in situ endlabelling technique called ‘ISEL+’ that identifies fragmented nuclear DNA in dying cells with increased sensitivity. The period encompassing murine cerebral cortical neurogenesis was examined, from embryonic days 10 through 18. Dying cells were rare at embryonic day 10, but by embryonic day 14, 70% of cortical cells were found to be dying. This number declined to 50% by embryonic day 18, and few dying cells were observed in the adult cerebral cortex. Surprisingly, while dying cells were observed throughout the cerebral cortical wall, the majority were found within zones of cell proliferation rather than in regions of postmitotic neurons. These observations suggest that multiple mechanisms may regulate programmed cell death in the developing cortex. Moreover, embryonic cell death could be an important factor enabling the selection of appropriate cortical cells before they complete their differentiation in postnatal life.

Characterization of proteases and nucleases associated with ethylene-induced programmed cell death in immature cucumber fruit

2015 ◽  
Vol 110 ◽  
pp. 190-196 ◽  
Author(s):  
Jin Su Lee ◽  
Brandon M. Hurr ◽  
Donald J. Huber ◽  
C.Eduardo Vallejos ◽  
Steven A. Sargent
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Cucumber Fruit

DNA degradation during programmed cell death in Phaseolus coccineus suspensor

2007 ◽  
Vol 45 (3-4) ◽  
pp. 221-227 ◽  
Author(s):  
Lara Lombardi ◽  
Nello Ceccarelli ◽  
Piero Picciarelli ◽  
Roberto Lorenzi
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Dna Degradation ◽  
Phaseolus Coccineus

scholarly journals Molecular cloning and characterization of CIDE-3, a novel member of the cell-death-inducing DNA-fragmentation-factor (DFF45)-like effector family

2003 ◽  
Vol 370 (1) ◽  
pp. 195-203 ◽  
Author(s):  
Liang LIANG ◽  
Mujun ZHAO ◽  
Zhenhua XU ◽  
Kazunari K. YOKOYAMA ◽  
Tsaiping LI
Keyword(s):  
Amino Acids ◽  
Cell Death ◽  
Small Intestine ◽  
Dna Fragmentation ◽  
Nuclear Dna ◽  
Fluorescent Protein ◽  
Reading Frame ◽  
Reverse Transcription Pcr ◽  
Green Fluorescent

DNA fragmentation is one of the critical steps in apoptosis, which is induced by DNA fragmentation factor (DFF). DFF is composed of two subunits, a 40kDa caspase-activated nuclease (DFF40) and a 45kDa inhibitor (DFF45). Recently a novel family of cell-death-inducing DFF45-like effectors (CIDEs) has been identified. Among CIDEs, two from human (CIDE-A and CIDE-B) and three from mouse (CIDE-A, CIDE-B and FSP27) have been reported. In this study human CIDE-3, a novel member of CIDEs, was identified upon sequence analysis of a previously unidentified cDNA that encoded a protein of 238 amino acids. It was shown to be a human homologue of mouse FSP27, and shared homology with the CIDE-N and CIDE-C domains of CIDEs. Apoptosis-inducing activity was clearly shown by DNA-fragmentation assay of the nuclear DNA of CIDE-3 transfected 293T cells. The expression pattern of CIDE-3 was different from that of CIDE-B. As shown by Northern-blot analysis, CIDE-3 was expressed mainly in human small intestine, heart, colon and stomach, while CIDE-B showed strong expression in liver and small intestine and at a lower level in colon, kidney and spleen. Green-fluorescent-protein-tagged CIDE-3 was revealed in some cytosolic corpuscles. Alternative splicing of the CIDE-3 gene was also identified by reverse transcription PCR, revealing that two transcripts, CIDE-3 and CIDE-3α, were present in HepG2 and A375 cells. CIDE-3 comprised a full-length open reading frame with 238 amino acids; in CIDE-3α exon 3 was deleted and it encoded a protein of 164 amino acids. Interestingly the CIDE-3α isoform still kept the apoptosis-inducing activity and showed the same pattern of subcellular localization as CIDE-3. Consistent with its chromosome localization at 3p25, a region associated with high frequency loss of heterozygosity in many tumours, CIDE-3 may play an important role in prevention of tumorigenesis.

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