scholarly journals Sphingolipid Effects on the Plasma Membrane Produced by Addition of Fumonisin B1 to Maize Embryos

Plants ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 150 ◽  
Author(s):  
Nora A. Gutiérrez-Nájera ◽  
Mariana Saucedo-García ◽  
Liliana Noyola-Martínez ◽  
Christian Vázquez-Vázquez ◽  
Silvia Palacios-Bahena ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Atpase Activity ◽  
Fusarium Verticillioides ◽  
Fumonisin B1 ◽  
Fold Increase ◽  
Membrane Properties ◽  
Ceramide Synthase ◽  
Animal Cells ◽  
Plasma Membrane Fluidity ◽  
Maize Embryos

Fumonisin B1 is a mycotoxin produced by Fusarium verticillioides that modifies the membrane properties from animal cells and inhibits complex sphingolipids synthesis through the inhibition of ceramide synthase. The aim of this work was to determine the effect of Fumonisin B1 on the plant plasma membrane when the mycotoxin was added to germinating maize embryos. Fumonisin B1 addition to the embryos diminished plasma membrane fluidity, increased electrolyte leakage, caused a 7-fold increase of sphinganine and a small decrease in glucosylceramide in the plasma membrane, without affecting phytosphingosine levels or fatty acid composition. A 20%–30% inhibition of the plasma membrane H+-ATPase activity was observed when embryos were germinated in the presence of the mycotoxin. Such inhibition was only associated to the decrease in glucosylceramide and the addition of exogenous ceramide to the embryos relieved the inhibition of Fumonisin B1. These results indicate that exposure of the maize embryos for 24 h to Fumonisin B1 allowed the mycotoxin to target ceramide synthase at the endoplasmic reticulum, eliciting an imbalance of endogenous sphingolipids. The latter disrupted membrane properties and inhibited the plasma membrane H+-ATPase activity. Altogether, these results illustrate the mode of action of the pathogen and a plant defense strategy.

Localization of Adenosine Triphosphatase Activity in the Phleom of Nicotiana Tabacum

1972 ◽  
Vol 30 ◽  
pp. 230-231
Author(s):  
James Cronshaw ◽  
Jamison E. Gilder
Keyword(s):  
Plasma Membrane ◽  
Atpase Activity ◽  
Adenosine Triphosphatase ◽  
Higher Plants ◽  
High Surface ◽  
Root Tip ◽  
Animal Cells ◽  
Physiological Processes ◽  
Tip Cells ◽  
Atpase Localization

Adenosine triphosphatase (ATPase) activity has been shown to be associated with numerous physiological processes in both plants and animal cells. Biochemical studies have shown that in higher plants ATPase activity is high in cell wall preparations and is associated with the plasma membrane, nuclei, mitochondria, chloroplasts and lysosomes. However, there have been only a few ATPase localization studies of higher plants at the electron microscope level. Poux (1967) demonstrated ATPase activity associated with most cellular organelles in the protoderm cells of Cucumis roots. Hall (1971) has demonstrated ATPase activity in root tip cells of Zea mays. There was high surface activity largely associated with the plasma membrane and plasmodesmata. ATPase activity was also demonstrated in mitochondria, dictyosomes, endoplasmic reticulum and plastids.

scholarly journals Comparison of plasma membrane H+-ATPase activity in vesicles obtained from dry and hydrated maize embryos

1998 ◽  
Vol 1414 (1-2) ◽  
pp. 175-187 ◽  
Author(s):  
Sobeida Sánchez-Nieto ◽  
Marietta Tuena de Gómez-Puyou ◽  
Rogelio Rodriguez-Sotres ◽  
Aquiles Carballo ◽  
Marina Gavilanes-Ruin
Keyword(s):  
Plasma Membrane ◽  
Atpase Activity ◽  
Maize Embryos

Plasma Membrane Fluidity and Surface Motility of Mouse C-1300 Neuroblastoma Cells

1973 ◽  
Vol 13 (2) ◽  
pp. 415-420
Author(s):  
P. M. COMOGLIO ◽  
G. FILOGAMO
Keyword(s):  
Plasma Membrane ◽  
Cell Membrane ◽  
Membrane Fluidity ◽  
Concanavalin A ◽  
Common Property ◽  
Neuroblastoma Cells ◽  
Metabolic Energy ◽  
Animal Cells ◽  
Plasma Membrane Fluidity ◽  
Polar Caps

Under suitable conditions, topographical redistribution of plasma membrane molecules with oligosaccharide residues specifically bound by Concanavalin-A can be induced on neuroblastoma C-1300 cells. This shows that transformed nerve cell membrane is fluid at 37 °C and provides further support for the suggestion that such fluidity may be a common property of all animal cells. As previously reported for mesenchymal cells (lymphocytes and fibroblasts), clustering of Concanavalin-A binding sites on the cell surface is dependent on temperature and on reagent concentration. The formation of larger aggregates, known as patches or polar caps, requires metabolic energy provided by the cell. In fibroblasts caps are formed in as little as 15-30 min. C-1300 neuroblastoma cells, however, need several hours of incubation before patches or, more rarely, single caps appear. The mechanism of formation of patches and caps is discussed with reference to cell membrane fluidity and the possibility that there exists a membrane motility characteristic of each cell type.

scholarly journals Ceramide Synthase-dependent Ceramide Generation and Programmed Cell Death

2011 ◽  
Vol 286 (18) ◽  
pp. 15929-15942 ◽  
Author(s):  
Thomas D. Mullen ◽  
Russell W. Jenkins ◽  
Christopher J. Clarke ◽  
Jacek Bielawski ◽  
Yusuf A. Hannun ◽  
...  
Keyword(s):  
Cell Death ◽  
Plasma Membrane ◽  
Programmed Cell Death ◽  
De Novo ◽  
Fumonisin B1 ◽  
Membrane Permeabilization ◽  
Ceramide Synthase ◽  
Plasma Membrane Permeabilization ◽  
Ceramide Generation ◽  
Uv C

The sphingolipid ceramide has been widely implicated in the regulation of programmed cell death or apoptosis. The accumulation of ceramide has been demonstrated in a wide variety of experimental models of apoptosis and in response to a myriad of stimuli and cellular stresses. However, the detailed mechanisms of its generation and regulatory role during apoptosis are poorly understood. We sought to determine the regulation and roles of ceramide production in a model of ultraviolet light-C (UV-C)-induced programmed cell death. We found that UV-C irradiation induces the accumulation of multiple sphingolipid species including ceramide, dihydroceramide, sphingomyelin, and hexosylceramide. Late ceramide generation was also found to be regulated by Bcl-xL, Bak, and caspases. Surprisingly, inhibition of de novo synthesis using myriocin or fumonisin B1 resulted in decreased overall cellular ceramide levels basally and in response to UV-C, but only fumonisin B1 inhibited cell death, suggesting the presence of a ceramide synthase (CerS)-dependent, sphingosine-derived pool of ceramide in regulating programmed cell death. We found that this pool did not regulate the mitochondrial pathway, but it did partially regulate activation of caspase-7 and, more importantly, was necessary for late plasma membrane permeabilization. Attempting to identify the CerS responsible for this effect, we found that combined knockdown of CerS5 and CerS6 was able to decrease long-chain ceramide accumulation and plasma membrane permeabilization. These data identify a novel role for CerS and the sphingosine salvage pathway in regulating membrane permeability in the execution phase of programmed cell death.

scholarly journals MPK6 Kinase Regulates Plasma Membrane H+-ATPase Activity in Cold Acclimation

2021 ◽  
Vol 22 (12) ◽  
pp. 6338
Author(s):  
Ilian Giordano Ponce-Pineda ◽  
Laura Carmona-Salazar ◽  
Mariana Saucedo-García ◽  
Dora Cano-Ramírez ◽  
Francisco Morales-Cedillo ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Atpase Activity ◽  
Cold Acclimation ◽  
Mitogen Activated Protein Kinase ◽  
Knock Out ◽  
Plasma Membrane Fluidity ◽  
Mapk Cascades ◽  
Cell Life ◽  
Mitogen Activated Protein ◽  
Key Enzyme

Cold and freezing stresses severely affect plant growth, development, and survival rate. Some plant species have evolved a process known as cold acclimation, in which plants exposed to temperatures above 0 °C trigger biochemical and physiological changes to survive freezing. During this response, several signaling events are mediated by transducers, such as mitogen activated protein kinase (MAPK) cascades. Plasma membrane H+-ATPase is a key enzyme for the plant cell life under regular and stress conditions. Using wild type and mpk3 and mpk6 knock out mutants in Arabidopsis thaliana, we explored the transcriptional, translational, and 14-3-3 protein regulation of the plasma membrane H+-ATPase activity under the acclimation process. The kinetic analysis revealed a differential profiling of the H+-ATPase activity depending on the presence or absence of MPK3 or MPK6 under non-acclimated or acclimated conditions. Negative regulation of the plasma membrane H+-ATPase activity was found to be exerted by MPK3 in non-acclimated conditions and by MPK6 in acclimated conditions, describing a novel form of regulation of this master ATPase. The MPK6 regulation involved changes in plasma membrane fluidity. Moreover, our results indicated that MPK6 is a critical regulator in the process of cold acclimation that leads to freezing tolerance and further survival.

scholarly journals Sonodynamic Treatment Induces Selective Killing of Cancer Cells in an In Vitro Co-Culture Model

Cancers ◽  
2021 ◽  
Vol 13 (15) ◽  
pp. 3852
Author(s):  
Federica Foglietta ◽  
Vanessa Pinnelli ◽  
Francesca Giuntini ◽  
Nadia Barbero ◽  
Patrizia Panzanelli ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Cancer Cells ◽  
Membrane Fluidity ◽  
Membrane Properties ◽  
Ros Production ◽  
Normal Cells ◽  
Plasma Membrane Fluidity ◽  
Cell Membrane Fluidity ◽  
Ht 29

Sonodynamic Therapy (SDT) is a new anticancer strategy based on ultrasound (US) technique and is derived from photodynamic therapy (PDT); SDT is still, however, far from clinical application. In order to move this therapy forward from bench to bedside, investigations have been focused on treatment selectivity between cancer cells and normal cells. As a result, the effects of the porphyrin activation by SDT on cancer (HT-29) and normal (HDF 106-05) cells were studied in a co-culture evaluating cell cytotoxicity, reactive oxygen species (ROS) production, mitochondrial function and plasma membrane fluidity according to the bilayer sonophore (BLS) theory. While PDT induced similar effects on both HT-29 and HDF 106-05 cells in co-culture, SDT elicited significant cytotoxicity, ROS production and mitochondrial impairment on HT-29 cells only, whereas HDF 106-05 cells were unaffected. Notably, HT-29 and HDF 106-05 showed different cell membrane fluidity during US exposure. In conclusion, our data demonstrate a marked difference between cancer cells and normal cells in co-culture in term of responsiveness to SDT, suggesting that this different behavior can be ascribed to diversity in plasma membrane properties, such as membrane fluidity, according to the BLS theory.

scholarly journals Developmental Toxicity of Mycotoxin Fumonisin B1 in Animal Embryogenesis: An Overview

Toxins ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 114 ◽  
Author(s):  
Chompunut Lumsangkul ◽  
Hsin-I Chiang ◽  
Neng-Wen Lo ◽  
Yang-Kwang Fan ◽  
Jyh-Cherng Ju
Keyword(s):  
Chemical Structure ◽  
Biosynthetic Pathway ◽  
De Novo ◽  
Developmental Toxicity ◽  
Fusarium Verticillioides ◽  
Fumonisin B1 ◽  
Primary Component ◽  
Ceramide Synthase ◽  
High Similarity ◽  
Developmental Abnormalities

A teratogenic agent or teratogen can disturb the development of an embryo or a fetus. Fumonisin B1 (FB1), produced by Fusarium verticillioides and F. proliferatum, is among the most commonly seen mycotoxins and contaminants from stale maize and other farm products. It may cause physical or functional defects in embryos or fetuses, if the pregnant animal is exposed to mycotoxin FB1. Due to its high similarity in chemical structure with lipid sphinganine (Sa) and sphingosine (So), the primary component of sphingolipids, FB1 plays a role in competitively inhibiting Sa and So, which are key enzymes in de novo ceramide synthase in the sphingolipid biosynthetic pathway. Therefore, it causes growth retardation and developmental abnormalities to the embryos of hamsters, rats, mice, and chickens. Moreover, maternal FB1 toxicity can be passed onto the embryo or fetus, leading to mortality. FB1 also disrupts folate metabolism via the high-affinity folate transporter that can then result in folate insufficiency. The deficiencies are closely linked to incidences of neural tube defects (NTDs) in mice or humans. The purpose of this review is to understand the toxicity and mechanisms of mycotoxin FB1 on the development of embryos or fetuses.

Hyperoxia reduces plasma membrane fluidity: a mechanism for endothelial cell dysfunction

1986 ◽  
Vol 60 (3) ◽  
pp. 826-835 ◽  
Author(s):  
E. R. Block ◽  
J. M. Patel ◽  
K. J. Angelides ◽  
N. P. Sheridan ◽  
L. C. Garg
Keyword(s):  
Endothelial Cells ◽  
Plasma Membrane ◽  
Pulmonary Artery ◽  
Atpase Activity ◽  
Membrane Fluidity ◽  
Atp Content ◽  
Aortic Endothelial Cells ◽  
Plasma Membrane Fluidity ◽  
High O2 ◽  
Aortic Endothelial

To evaluate the relative contributions of three possible mechanisms that can be advanced to explain the observation that hyperoxia decreases serotonin uptake by endothelial cells, we examined the effect of high O2 tensions on Na+-K+-ATPase activity, ATP content, and plasma membrane fluidity in cultured endothelial cells. Confluent monolayers of pulmonary artery and aortic endothelial cells were exposed to 95% O2 (hyperoxia) or 20% O2 (controls) in 5% CO2 at 1 ATA for 4–42 h. Exposure to high O2 tensions had no effect on Na+-K+-ATPase activity or ATP content in pulmonary artery or aortic endothelial cells in culture. However, hyperoxia decreased the fluidity of the plasma membrane of pulmonary artery and aortic endothelial cells in culture, and the time course for the decrease in fluidity parallels that of the hyperoxic inhibition of serotonin transport. These results indicate that hyperoxia decreases fluidity in the hydrophobic core of the plasma membranes of cultured endothelial cells. Such decreases in plasma membrane fluidity may be responsible for hyperoxia-induced alterations in membrane function including decreases in transmembrane transport of amines.

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