scholarly journals Programmed Cell Death Facilitates the Formation of Unisexual Male and Female Flowers in Persimmon (Diospyros kaki Thunb.)

Agronomy ◽  
2020 ◽  
Vol 10 (2) ◽  
pp. 234
Author(s):  
Wang ◽  
Li ◽  
Suo ◽  
Han ◽  
Diao ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Quantitative Polymerase Chain Reaction ◽  
Normal Growth ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Diospyros Kaki ◽  
Male And Female ◽  
Floral Buds ◽  
Unisexual Flowers ◽  
Normal Flower

Most varieties of persimmon (Diospyros kaki Thunb.) are gynoecious, while just a few are either monoecious, androgynomonoecious, or androecious. Persimmon flowers initially contain the original androecium and gynoecium followed by arrest of either pistil or stamen primordia before maturity. Abortion of inappropriate primordium in persimmon may be related to programmed cell death (PCD). To test this hypothesis, hematoxylin and eosin (H&E) staining, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay, cyt-c immunohistochemistry (IHC) assay, transmission electron microscopy (TEM) observation, and real-time quantitative polymerase chain reaction (RT-qPCR) were used to clarify the occurrence and molecular regulatory mechanism of PCD in male and female floral buds during the 14 days prior to the second crucial morphological stage when inappropriate sexual primordia were arrested to form unisexual flowers. Accordingly, dead cells in inappropriate sex organs were largely accumulated during the microsporocyte and macrosporocyte period of male and female floral buds, respectively. This may explain the abortion of inappropriate sex organs, leading to unisexual flowers. PCD is necessary for normal growth and development in persimmons, as dead cells could also be observed in the normal flower organs. High levels of a gene homologous to AMC9 may have accelerated the arrest of the pistil primordium during differentiation, leading to male unisexual flowers, and high levels of genes homologous to MeGI, BAG5, AifA, and HSP70 in female floral buds were positively correlated with the arrest of stamen primordium. Future studies may try to transform unisexual flowers into hermaphroditic flowers by the regulation of PCD artificially, which will be helpful to the controlled pollination experiments.

scholarly journals Flight muscles degenerate by programmed cell death after migration in the wheat aphid, Sitobion avenae

2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Honglin Feng ◽  
Xiao Guo ◽  
Hongyan Sun ◽  
Shuai Zhang ◽  
Jinghui Xi ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Molecular Mechanism ◽  
Differentially Expressed Genes ◽  
Flight Muscle ◽  
Sitobion Avenae ◽  
Differentially Expressed ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Muscle Degeneration ◽  
Flight Muscles

Abstract Objective Previous studies showed that flight muscles degenerate after migration in some aphid species; however, the underlying molecular mechanism remains virtually unknown. In this study, using the wheat aphid, Sitobion avenae, we aim to investigate aphid flight muscle degeneration and the underlying molecular mechanism. Results Sitobion avenae started to differentiate winged or wingless morphs at the second instar, the winged aphids were fully determined at the third instar, and their wings were fully developed at the fourth instar. After migration, the aphid flight muscles degenerated via programmed cell death, which is evidenced by a Terminal deoxynucleotidyl transferase dUTP-biotin nick-end labeling assay. Then, we identified a list of differentially expressed genes before and after tethered flights using differential-display reverse transcription-PCR. One of the differentially expressed genes, ubiquitin-ribosomal S27a, was confirmed using qPCR. Ubiquitin-ribosomal S27a is drastically up regulated following the aphids’ migration and before the flight muscle degeneration. Our data suggested that aphid flight muscles degenerate after migration. During flight muscle degeneration, endogenous proteins may be degraded to reallocate energy for reproduction.

scholarly journals Flight muscles degenerate by programmed cell death after migration in the wheat aphid, Sitobion avenae

2019 ◽  
Author(s):  
Honglin Feng ◽  
Xiao Guo ◽  
Hongyan Sun ◽  
Shuai Zhang ◽  
Jinghui Xi ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Differentially Expressed Genes ◽  
Flight Muscle ◽  
Aphid Species ◽  
Sitobion Avenae ◽  
Differentially Expressed ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Muscle Degeneration ◽  
Flight Muscles

Abstract Objective Previous studies showed that flight muscles degenerate after migration in some aphid species; however, the underlying molecular mechanism remains virtually unknown. In this study, using the wheat aphid, Sitobion avenae , we aim to investigate aphid flight muscle degeneration and the underlying molecular mechanism.Results S. avenae started to differentiate winged or wingless lines at the second instar, the winged aphids were fully determined at the third instar, and their wings were fully developed at the fourth instar. After migration, the aphid flight muscles degenerated via programmed cell death, which is evidenced by a Terminal deoxynucleotidyl transferase dUTP-biotin nick end labeling assay. Then, we identified a list of differentially expressed genes before and after tethered flights using differential-display reverse transcription-PCR. One of the differentially expressed genes, ubiquitin-ribosomal S27a, was confirmed using qPCR. Ubiquitin-ribosomal S27a is drastically up regulated following the aphids’ migration and before the flight muscle degeneration. Our data suggested that aphid flight muscles degenerate after migration. During flight muscle degeneration, endogenous proteins may be degraded to reallocate energy for reproduction.

Transcriptome sequencing and comparative analysis between male and female floral buds of the persimmon (Diospyros kaki Thunb.)

2019 ◽  
Vol 246 ◽  
pp. 987-997 ◽  
Author(s):  
Shuzhan Li ◽  
Peng Sun ◽  
Gaigai Du ◽  
Liyuan Wang ◽  
Huawei Li ◽  
...  
Keyword(s):  
Comparative Analysis ◽  
Transcriptome Sequencing ◽  
Diospyros Kaki ◽  
Male And Female ◽  
Floral Buds

Apoptosis after traumatic human spinal cord injury

1998 ◽  
Vol 5 (4) ◽  
pp. E1 ◽  
Author(s):  
Evelyne Emery ◽  
Philipp Aldana ◽  
Mary Bartlett Bunge ◽  
William Puckett ◽  
Anu Srinivasan ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Positive Staining ◽  
Apoptotic Cells ◽  
Nuclear Staining ◽  
Human Spinal Cord ◽  
Cord Injury

Object Apoptosis is a form of programmed cell death seen in a variety of developmental and disease states, including traumatic injuries. The main objective of this study was to determine whether apoptosis is observed after human spinal cord injury (SCI). The spatial and temporal expression of apoptotic cells as well as the nature of the cells involved in programmed cell death were also investigated. Methods The authors examined the spinal cords of 15 patients who died between 3 hours and 2 months after a traumatic SCI. Apoptotic cells were found at the edges of the lesion epicenter and in the adjacent white matter, particularly in the ascending tracts, by using histological (cresyl violet, hematoxylin and eosin) and nuclear staining (Hoechst 33342). The suspected presence of apoptotic cells was supported by staining with the terminal deoxynucleotidyl transferase-mediated biotinylated-deoxyuridinetriphosphate nick-end labeling technique and confirmed by immunostaining for the processed form of caspase-3 (CPP-32), a member of the interleukin-1-beta-converting enzyme/Caenorhabditis elegans D 3 family of proteases that plays an essential role in programmed cell death. Apoptosis in this series of human SCIs was a prominent pathological finding in 14 of the 15 spinal cords examined when compared with five uninjured control spinal cords. To determine the type of cells undergoing apoptosis, the authors immunostained specimens with a variety of antibodies, including glial fibrillary acidic protein, 2,′3′-cyclic nucleotide 3′-phosphohydrolase (CNPase), and CD45/68. Oligodendrocytes stained with CNPase and a number of apoptotic nuclei colocalized with positive staining for this antibody. Conclusions These results support the hypothesis that apoptosis occurs in human SCIs and is accompanied by the activation of CPP-32 of the cysteine protease family. This mechanism of cell death contributes to the secondary injury processes seen after human SCI and may have important clinical implications for the further development of protease inhibitors to prevent programmed cell death.

scholarly journals “Programmed Cell Death: A Process of Death for Survival” – How Far Terminology Pertinent for Cell Death in Unicellular Organisms

2018 ◽  
Vol 11 ◽  
pp. 117906601879025 ◽  
Author(s):  
Shiv Shanker Pandey ◽  
Samer Singh ◽  
Chandramani Pathak ◽  
Budhi Sagar Tiwari
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Normal Growth ◽  
Death Process ◽  
Target Cells ◽  
Dna Ladder ◽  
Cell Death Process ◽  
Unicellular Organisms ◽  
Multicellular Organisms ◽  
Dna Nicks

Programmed cell death (PCD) is genetically regulated phenomenon of selective elimination of target cells that are either under pathological conditions or unwanted for organism’s normal growth and development due to other reasons. The process although being genetically controlled is physiological in nature that renders some hallmarks like blebs in the cell membrane, lobe formation in nuclear membrane, DNA nicks resulting to DNA ladder of 200 bp, and downstream activation of caspases. Moreover, as the process refers to the death of “targeted cell”, the term is exclusively suitable for multicellular organisms. Number of reports advocate similar type of cell death process in unicellular organisms. As cell death in unicellular organisms is also reflected by the signature of PCD obtained in metazoans, such cell death has been grouped under the broad category of PCD. It is pertinent to mention that by definition a unicellular organism is made of a single cell wherein it carries out all of its life processes. Using the term “Programmed Cell Death” with a preset “survival strategy of the organism” for unicellular organisms looks misnomer. Therefore, this correspondence argues and requests recommendation committee on cell death to revisit for the nomenclature of the cell death process in the unicellular organisms.

Assessment of apoptotic cells in the wall of thrombophlebitic saphenous vein

2015 ◽  
Vol 31 (3) ◽  
pp. 216-221 ◽  
Author(s):  
Hu Li ◽  
Wei Han ◽  
Lei Wang ◽  
Haibo Chu ◽  
Yongbo Xu ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Varicose Veins ◽  
Critical Role ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Control Group ◽  
Apoptotic Cells ◽  
High Power Field ◽  
Saphenous Veins ◽  
Significant Difference

Introduction Programmed cell death plays a critical role in various physiological processes. In the present study, we investigated its possible pathogenic role in primary varicose veins. We studied histological changes in surgical specimens from thrombophlebitic saphenous veins. In thrombophlebitic saphenous, varicose, and healthy veins, we also determined the number of apoptotic cells, and investigated apoptosis in the role of the pathogenesis of varicose veins. Methods Forty-four specimens of thrombophlebitic saphenous veins and simple varicose veins were collected. Thirteen samples of normal great saphenous veins were also collected (control group). Apoptosis of venous walls was determined by terminal deoxynucleotidyl transferase-mediated nick-end labeling (TUNEL) and immunofluorescence methods. The corpuscular number per high-power field was counted under light microscopy. Results A significantly higher apoptotic ratio of the intima and media were observed in control veins as compared with thrombophlebitic saphenous veins and simple varicose veins ( p < 0.01). A significant difference was not observed between thrombophlebitic saphenous veins and simple varicose veins ( p > 0.05). A significant difference was not seen between the intima and media of the three groups ( p > 0.05). Conclusion In the walls of thrombophlebitic saphenous veins and varicose veins, the apoptotic indices were clearly decreased. The results suggest that the process of programmed cell death was inhibited in walls of thrombophlebitic saphenous veins and varicose veins.

scholarly journals Retro-retinoids in regulated cell growth and death.

1996 ◽  
Vol 184 (2) ◽  
pp. 549-555 ◽  
Author(s):  
M J O'Connell ◽  
R Chua ◽  
B Hoyos ◽  
J Buck ◽  
Y Chen ◽  
...  
Keyword(s):  
Signal Transduction ◽  
T Cells ◽  
Cell Death ◽  
Transcription Factors ◽  
Programmed Cell Death ◽  
Vitamin A ◽  
Dna Cleavage ◽  
Second Messenger ◽  
Terminal Deoxynucleotidyl Transferase ◽  
General Notion

Vitamin A serves as a prohormone from which three classes of active metabolites are derived: the aldehydes, the carboxylic acids, and the retro-retinoids. Although these three classes are united under the rubric of signal transduction, they act by different molecular mechanisms: the 11-cis-retinaldehydes combine with opsin to form the universal visual pigments and the retinoic acids form ligands for transcription factors, whereas the retro-retinoids, as shown here, intersect with signal transduction at a cytoplasmic or membrane site. The retro-retinoid, anhydroretinol (AR), has long been known to act as a growth inhibitor in lymphocytes, whereas 14-hydroxy-4,14-retro-retinol (14-HRR) is required for normal lymphocyte proliferation. A mutually reversible relationship exists between these two retro-retinoids as one can reverse the effects of the other when given in pharmacological doses. The common explanation for reversible inhibition is competition for a shared receptor. We now provide evidence that when AR is given to T cells unmitigated by 14-HRR, rapid cell death can occur. The circumstances are closely related to nonclassical forms of apoptosis: within 2 h of AR administration the T cells undergo widespread morphological changes, notably surface blebbing and ballooning and, inevitably, bursting. In contrast, nuclear changes are comparatively mild, as indicated by absence of chromatin condensation and overt DNA cleavage to discrete nucleosomal fragments, although DNA nicks are readily discernible by terminal deoxynucleotidyl transferase assay. What further distinguishes the AR-induced form of apoptosis from classical ones is a lack of requirements of messenger RNA and protein synthesis, suggesting that the events leading to cell death are primarily initiated and play themselves out in the cytoplasm. This view is further reinforced by the finding that herbimycin A can prevent the onset of programmed cell death. The importance of our findings is that they strongly suggest a second messenger role for vitamin A metabolites in the cytoplasmic realm that has not been seen previously. These findings are entirely compatible with a general notion that in a cell requiring multiple coordinated signals for survival, the provision of an unbalanced signal can initiate programmed cell death. Collectively, our data also challenge the paradigm that retinoids (outside vision) solely mediate their function via the steroid/ retinoic acid receptor family of nuclear transcription factors. Instead, a mode of action in the cytoplasmic realm akin to one attributed to other small lipophilic second messenger molecules, such as diacyl glycerol or ceramide, may apply to retro-retinoids.

scholarly journals Caspofungin Kills Candida albicans by Causing both Cellular Apoptosis and Necrosis

2012 ◽  
Vol 57 (1) ◽  
pp. 326-332 ◽  
Author(s):  
Binghua Hao ◽  
Shaoji Cheng ◽  
Cornelius J. Clancy ◽  
M. Hong Nguyen
Keyword(s):  
Cell Death ◽  
Candida Albicans ◽  
Programmed Cell Death ◽  
Membrane Integrity ◽  
Annexin V ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Dapi Staining ◽  
Content Type ◽  
Glucan Synthesis ◽  
Apoptosis And Necrosis

ABSTRACTCaspofungin exerts candidacidal activity by inhibiting cell wall (1,3)-β-d-glucan synthesis. We investigated the physiologic mechanisms of caspofungin-inducedCandida albicanscell death. Apoptosis (programmed cell death) and necrosis were studied afterC. albicansSC5314 cells were exposed to caspofungin at 0.06, 0.125, and 0.5 μg/ml (0.5×, 1×, and 4× the MIC, respectively) for 3 h. Caspofungin at 0.125 and 0.5 μg/ml reduced cellular viability by >50%, as measured by colony counts and methylene blue exclusion. Apoptosis and necrosis were demonstrated by annexin V and propidium iodide staining for phosphatidylserine externalization and loss of membrane integrity, respectively. At all concentrations of caspofungin, 20 to 25% and 5 to 7% ofC. albicanscells exhibited early apoptosis and late apoptosis/necrosis, respectively (Pvalue was not significant [NS]). Necrosis, on the other hand, was significantly greater at 0.125 (43%) and 0.5 (48%) μg/ml than at 0.06 μg/ml (26%) (Pvalues of 0.003 and 0.003, respectively). The induction of apoptosis at concentrations less than or equal to the MIC was corroborated by dihydrorhodamine 123 (DHR-123) and dihydroethidium (DHE) staining (reactive oxygen species production), JC-1 staining (mitochondrial membrane potential dissipation), and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) and 4′,6-diamidino-2-phenylindole dihydrochloride (DAPI) staining (DNA damage and nuclear fragmentation). Moreover, electron microscopy of cells exposed to 0.125 μg/ml of caspofungin showed hallmark apoptotic features like chromatin margination and condensation and nuclear blebs. Apoptosis was associated with metacaspase 1 activation, as demonstrated by D2R staining. Caspofungin exerts activity againstC. albicansby directly killing cells (resulting in necrosis) and causing others to undergo programmed cell death (apoptosis). Apoptosis is initiated at subinhibitory concentrations, suggesting that strategies to target this process may augment the benefits of antifungal agents.

scholarly journals Structural Modifications and Programmed Cell Death of Chili Pepper Fruit Related to Resistance Responses to Colletotrichum gloeosporioides Infection

2004 ◽  
Vol 94 (12) ◽  
pp. 1295-1304 ◽  
Author(s):  
Kwang-Hyung Kim ◽  
Jae-Bok Yoon ◽  
Hyo-Guen Park ◽  
Eun Woo Park ◽  
Young Ho Kim
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Laser Scanning ◽  
Structural Changes ◽  
Colletotrichum Gloeosporioides ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Confocal Laser ◽  
In Planta ◽  
Pepper Fruit ◽  
Nuclear Modifications

Postharvest (detached) and in planta (attached) fruits of pepper plants, Capsicum annuum cv. Jejujaerae (susceptible) and Capsicum baccatum cv. PBC80 (resistant), inoculated with the anthracnose pathogen Colletotrichum gloeosporioides were examined using light, confocal laser scanning, and electron microscopy to compare the cytological differences between the compatible and incompatible interactions. In nonwound inoculation of postharvest pepper fruit, resistant pepper tissues showed a significant increase in the thickness of the cuticle layer compared with that of the susceptible and noninoculated fruit. Cytological features of programmed cell death (PCD) were observed in the resistant pepper fruit with postharvest inoculation, and these were characterized by positive responses to terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling. The oligonucleosomal fragments of DNA were confirmed electrophoretically as DNA laddering. The PCD-positive responses occurred around the inoculation sites early in in planta wound inoculation in the resistant pepper. Nuclear modifications and structural changes of hypersensitivity were also observed in the resistant fruit, including separation of the plasma membrane from the cell wall, dilation of the endoplasmic reticulum, accumulation of electron-dense inclusions in vacuoles, and cytoplasmic vacuolization accompanying fragmentation of the cytoplasm. These structural changes may also implicate PCD-like host responses. In addition, in planta wound inoculation resulted in cell enlargement and cell division during the later stages of infection to form a periderm-like boundary layer around the inoculation site.

scholarly journals Role of microRNA 4717, its effects on programmed cell death protein-1 in hepatitis B infection, and interaction between PDCD1 and miR-4717

2020 ◽  
Vol 18 ◽  
pp. 205873922093460
Author(s):  
Junhua Li ◽  
Andong Li
Keyword(s):  
Cell Death ◽  
Hepatitis B ◽  
Programmed Cell Death ◽  
Quantitative Polymerase Chain Reaction ◽  
Nucleotide Polymorphisms ◽  
Tissue Samples ◽  
Expression Levels ◽  
Si Rna ◽  
Cell Death Protein

It is suggested that programmed cell death protein-1 (PD-1) is involved in hepatitis B virus (HBV) infection, the leading cause of hepatocellular carcinoma globally. This study was multi-aimed, that is, to investigate the role of microRNA (miR) 4717 and its target, PD-1 and to determine how the rs10204525 polymorphism in the 3′ untranslated region (3′UTR) of PD-1 affects its interaction with miR-4717. The expression levels of miR-4717 with various single-nucleotide polymorphisms were measured by reverse transcription–quantitative polymerase chain reaction (RT-qPCR). A total of 54 tissue samples from HBV-infected individuals were collected, genotyped, and categorized into three groups; AA (n = 32), AG (n = 18), and GG (n = 4). The expression levels of gene PDCD1 and its corresponding PD-1 protein were significantly declined in the AA group as compared to AG and GG groups. There was a negative linear association between PDCD1 and miR-4717 in the tissue samples. HEPG2 cells transfected with an miR-4717 mimic or PD-1 small interfering (si)RNA exhibited significantly reduced expression levels of PDCD1 and PD-1, whereas cells transfected with an inhibitor of miR-4717 demonstrated greater expression levels of PDCD1 and PD-1 compared with the scramble control. In addition, cell viability and apoptosis were assessed in cells transfected with an miR-4717 mimic, PD-1 siRNA, or an miR-4717 inhibitor. Results revealed that treatment with the miR-4717 mimic or PD-1 siRNA enhanced viability of cells and reduced apoptosis. The results of this study suggest that rs10204525 polymorphism interferes with the interaction between PD-1 and miR-4717 and therefore induces apoptosis in liver cancer cells.

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