Leafy Spurge (Euphorbia esula) Cell Cultures for Screening Deleterious Rhizobacteria

Weed Science ◽  
1994 ◽  
Vol 42 (2) ◽  
pp. 310-315 ◽  
Author(s):  
Thouraya Souissi ◽  
Robert J. Kremer
Keyword(s):  
Cell Death ◽  
Cell Cultures ◽  
Screening Method ◽  
Leafy Spurge ◽  
Cellular Level ◽  
Biocontrol Agents ◽  
Physical Contact ◽  
Host Pathogen Interaction ◽  
Deleterious Rhizobacteria ◽  
Callus Tissues

Bioassays using cell cultures and callus tissues of leafy spurge were devised to evaluate the potential of rhizobacteria as biocontrol agents. Rhizobacteria isolated from roots of leafy spurge seedlings were screened in suspension-cultured leafy spurge cells. Cell viability was assessed using the Evan's blue bioassay 48 h after bacterial inoculation. Among the 30 isolates tested, LS102 and LS105 consistently caused intensive cell death determined by measuring the A630of the inoculated cell cultures. Cell death was 2.5 to 3 times higher in cultures inoculated with LS105 and LS102, respectively, than in the control. Population levels of the two isolates within cell cultures and callus tissues of leafy spurge increased during the first 48 h. Leafy spurge callus tissues were inoculated with rhizobacteria either directly or by using the Host Pathogen Interaction System (HPIS). The latter exposes calli to bacteria without any physical contact. LS102 caused cellular leakage and eventually death of the callus tissue. Callus growth was reduced by about 30 to 70% when exposed to LS102 and LS105, respectively. Results suggest that these two isolates may affect leafy spurge at the cellular level by different mechanisms. A screening method based on cell cultures and callus tissues offers a good and rapid technique for detecting deleterious rhizobacteria with potential as biocontrol agents for leafy spurge.

1-Butanol triggers programmed cell death in Populus euphratica cell cultures

2014 ◽  
Vol 74 (1) ◽  
pp. 33-45
Author(s):  
Jing Zhang ◽  
Yicheng Yu ◽  
Zongyun Li ◽  
Cunhua Sun ◽  
Jian Zhang ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Cell Cultures ◽  
Populus Euphratica

scholarly journals NMDA Receptor-Mediated Neuroprotective Effect of theScutellaria baicalensisGeorgi Extract on the Excitotoxic Neuronal Cell Death in Primary Rat Cortical Cell Cultures

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Jinsong Yang ◽  
Xiaohong Wu ◽  
Haogang Yu ◽  
Xinbiao Liao ◽  
Lisong Teng
Keyword(s):  
Cell Death ◽  
Nmda Receptor ◽  
Cell Cultures ◽  
Neuroprotective Effect ◽  
Neuronal Cell Death ◽  
Cortical Cell ◽  
Neuronal Cell ◽  
Ethanol Extract ◽  
Phytochemical Analysis ◽  
Cortical Cell Cultures

The objective of the current research work was to evaluate the neuroprotective effect of the ethanol extract ofScutellaria baicalensis(S.B.) on the excitotoxic neuronal cell death in primary rat cortical cell cultures. The inhibitory effects of the extract were qualitatively and quantitatively estimated by phase-contrast microscopy and lactate dehydrogenase (LDH) assays. The extract exhibited a potent and dose-dependent inhibition of the glutamate-induced excitotoxicity in the culture media. Further, using radioligand binding assays, it was observed that the inhibitory effect of the extract was more potent and selective for the N-methyl-D-aspartate (NMDA) receptor-mediated toxicity. The S.B. ethanol extract competed with [3H] MDL 105,519 for the specific binding to the NMDA receptor glycine site with 50% inhibition occurring at 35.1 μg/mL. Further, NMDA receptor inactivation by the S.B. ethanol extract was concluded from the decreasing binding capability of [3H]MK-801 in the presence of the extract. Thus, S.B. extract exhibited neuroprotection against excitotoxic cell death, and this neuroprotection was mediated through the inhibition of NMDA receptor function by interacting with the glycine binding site of the NMDA receptor. Phytochemical analysis of the bioactive extract revealed the presence of six phytochemical constituents including baicalein, baicalin, wogonin, wogonoside, scutellarin, and Oroxylin A.

scholarly journals Internucleosomal DNA cleavage and neuronal cell survival/death

1993 ◽  
Vol 122 (3) ◽  
pp. 523-532 ◽  
Author(s):  
A Batistatou ◽  
LA Greene
Keyword(s):  
Cell Death ◽  
Cell Survival ◽  
Pc12 Cells ◽  
Dna Fragmentation ◽  
Cell Cultures ◽  
Pc12 Cell ◽  
Dna Cleavage ◽  
Sympathetic Neurons ◽  
Term Survival ◽  
Serum Withdrawal

Serum-free PC12 cell cultures have been used to study the mechanisms of neuronal death after neurotrophic factor deprivation. We previously reported that PC12 cells undergo "apoptotic" internucleosomal DNA cleavage after withdrawal of trophic support. Here, we have used a sensitive method to detect PC12 cell DNA fragmentation within three hrs of serum removal and have exploited this assay to examine several aspects regarding the mechanisms of neuronal survival/death. Major advantages of this assay are that it permits acute experiments to be performed well before other manifest signs of cell death and under conditions that cannot be applied chronically. We find that this apopotic DNA fragmentation is distinct from the random DNA degradation that occurs during necrotic death. Major observations include the following: (a) There is a good correlation between the ability of trophic substances to promote PC12 cell survival and to inhibit early DNA fragmentation. (b) Phorbol ester, an activator of PKC, acutely suppresses DNA fragmentation, but does not promote long-term survival or inhibition of endonuclease activity when applied chronically due to its downregulation of PKC. (c) Cells undergoing apoptosis within 3 h of serum withdrawal have a "commitment point" of only 1.0-1.5 h beyond which they can no longer be rescued by NGF. (d) Aurin, a non-carboxylic analog of the endonuclease inhibitor ATA, also inhibits DNA fragmentation and promotes short-term survival of PC12 cells. (e) Macromolecular synthesis is not required for DNA fragmentation or for NGF to prevent this event. (f) Extracellular Ca2+ is not required for internucleosomal DNA cleavage caused by serum withdrawal or for suppression of this by NGF. (g) DNA fragmentation can also be detected in cultures of rat sympathetic neurons as early as 10 h after removal of NGF. As in PC12 cell cultures, this precedes morphological signs of cell death.

scholarly journals BAX INHIBITOR-1 Is Required for Full Susceptibility of Barley to Powdery Mildew

2010 ◽  
Vol 23 (9) ◽  
pp. 1217-1227 ◽  
Author(s):  
Ruth Eichmann ◽  
Melanie Bischof ◽  
Corina Weis ◽  
Jane Shaw ◽  
Christophe Lacomme ◽  
...  
Keyword(s):  
Cell Death ◽  
Powdery Mildew ◽  
Gene Silencing ◽  
Defense Responses ◽  
Negative Control ◽  
Cellular Level ◽  
Virus Induced Gene Silencing ◽  
Powdery Mildew Fungus ◽  
Basal Resistance ◽  
Enhanced Resistance

BAX INHIBITOR-1 (BI-1) is one of the few proteins known to have cross-kingdom conserved functions in negative control of programmed cell death. Additionally, barley BI-1 (HvBI-1) suppresses defense responses and basal resistance to the powdery mildew fungus Blumeria graminis f. sp. hordei and enhances resistance to cell death–provoking fungi when overexpressed in barley. Downregulation of HvBI-1 by transient-induced gene silencing or virus-induced gene silencing limited susceptibility to B. graminis f. sp. hordei, suggesting that HvBI-1 is a susceptibility factor toward powdery mildew. Transient silencing of BI-1 did not limit supersusceptibility induced by overexpression of MLO. Transgenic barley plants harboring an HvBI-1 RNA interference (RNAi) construct displayed lower levels of HvBI-1 transcripts and were less susceptible to powdery mildew than wild-type plants. At the cellular level, HvBI-1 RNAi plants had enhanced resistance to penetration by B. graminis f. sp. hordei. These data support a function of BI-1 in modulating cell-wall-associated defense and in establishing full compatibility of B. graminis f. sp. hordei with barley.

scholarly journals Heat-shock proteases promote survival of Pseudomonas aeruginosa during growth arrest

2020 ◽  
Vol 117 (8) ◽  
pp. 4358-4367 ◽  
Author(s):  
David W. Basta ◽  
David Angeles-Albores ◽  
Melanie A. Spero ◽  
John A. Ciemniecki ◽  
Dianne K. Newman
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Cell Death ◽  
Heat Shock ◽  
Protein Aggregation ◽  
Protein Quality ◽  
Growth Arrest ◽  
Cellular Level ◽  
Secondary Response ◽  
Bacterial Cells ◽  
Encoding Genes

When nutrients in their environment are exhausted, bacterial cells become arrested for growth. During these periods, a primary challenge is maintaining cellular integrity with a reduced capacity for renewal or repair. Here, we show that the heat-shock protease FtsH is generally required for growth arrest survival of Pseudomonas aeruginosa, and that this requirement is independent of a role in regulating lipopolysaccharide synthesis, as has been suggested for Escherichia coli. We find that ftsH interacts with diverse genes during growth and overlaps functionally with the other heat-shock protease-encoding genes hslVU, lon, and clpXP to promote survival during growth arrest. Systematic deletion of the heat-shock protease-encoding genes reveals that the proteases function hierarchically during growth arrest, with FtsH and ClpXP having primary, nonredundant roles, and HslVU and Lon deploying a secondary response to aging stress. This hierarchy is partially conserved during growth at high temperature and alkaline pH, suggesting that heat, pH, and growth arrest effectively impose a similar type of proteostatic stress at the cellular level. In support of this inference, heat and growth arrest act synergistically to kill cells, and protein aggregation appears to occur more rapidly in protease mutants during growth arrest and correlates with the onset of cell death. Our findings suggest that protein aggregation is a major driver of aging and cell death during growth arrest, and that coordinated activity of the heat-shock response is required to ensure ongoing protein quality control in the absence of growth.

scholarly journals Oxidative burst and cell death induced by b-quercinin and zoospores of Phytophthora quercina in tobacco cell cultures

2017 ◽  
Vol 38 (SI 2 - 6th Conf EFPP 2002) ◽  
pp. 446-448 ◽  
Author(s):  
J. Koehl ◽  
E.F. Elstner ◽  
W. Oßwald ◽  
I. Heiser
Keyword(s):  
Cell Death ◽  
Cell Suspension ◽  
Cell Cultures ◽  
Oxidative Burst ◽  
Mode Of Action ◽  
Cell Suspension Cultures ◽  
Suspension Cultures ◽  
Tobacco Cell ◽  
Tobacco Cell Suspension

Mode of action of β-quercinin, a novel elicitin on tobacco cell suspension cultures (cvs. Bel B and Bel W3) was investigated by measuring the oxidative burst and cell death in these cell cultures. β-quercinin induced an oxidative burst comparable to that excited by zoospores from P. quercina. Adding superoxidedismutase, catalase and diphenyleneiodonium to elicited cell cultures, it could be demonstrated, that the induction of cell death in tobacco cell cultures is not correlated to the oxidative burst.

Anandamide-Induced Cell Death: Dual Effects in Primary Rat Decidual Cell Cultures

Placenta ◽  
2009 ◽  
Vol 30 (8) ◽  
pp. 686-692 ◽  
Author(s):  
B.M. Fonseca ◽  
G. Correia-da-Silva ◽  
N.A. Teixeira
Keyword(s):  
Cell Death ◽  
Cell Cultures ◽  
Decidual Cell
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