scholarly journals Rearing temperature and fatty acid supplementation jointly affect membrane fluidity and heat tolerance inDaphnia

2018 ◽  
Author(s):  
D. Martin-Creuzburg ◽  
B.L. Coggins ◽  
D. Ebert ◽  
L.Y. Yampolsky
Keyword(s):  
Fatty Acid ◽  
Membrane Fluidity ◽  
Relative Abundance ◽  
Heat Tolerance ◽  
Fluorescence Polarization ◽  
Membrane Properties ◽  
Membrane Phospholipids ◽  
Homeoviscous Adaptation ◽  
Body Tissues ◽  
Adaptation Hypothesis

AbstractThe homeoviscous adaptation hypothesis states that the relative abundance of polyunsaturated fatty acids (PUFA) decreases in the membrane phospholipids of ectothermic organisms at higher temperatures to maintain vital membrane properties. We hypothesized that the well-documented reduced heat tolerance of cold-rearedDaphniais due to the accumulation of PUFA in their body tissues and that heat-rearedDaphniacontain reduced amounts of PUFA even when receiving a high dietary supply of PUFA. InDaphniareared at 15°C, supplementation of a PUFA-deficient food with the long-chain PUFA eicosapentaenoic acid (EPA) resulted in an increase in the relative abundance of EPA in body tissues and a decrease in heat tolerance. However, the same was observed inDaphniareared at 25°C, indicating that the ability of heat-acclimatedDaphniato adjust EPA body concentrations is limited when exposed to high dietary EPA concentrations.Daphniareared at 25°C showed the lowest change in membrane fluidity, measured as fluorescence polarization. ForDaphniareared at three different temperatures, thermal tolerance (time to immobility at a lethally high temperature) and increasing dietary EPA concentrations correlated with fluorescence polarization and the degree of fatty acid unsaturation. Overall, our results support the homeoviscous adaptation hypothesis by showing that cold-rearedDaphnia,which accumulate PUFA within their tissues, are more susceptible to heat than hot-rearedDaphnia,which contain less PUFA.

Molecular control of membrane properties during temperature acclimation. Fatty acid desaturase regulation of membrane fluidity in acclimating Tetrahymena cells

Biochemistry ◽  
1976 ◽  
Vol 15 (24) ◽  
pp. 5218-5227 ◽  
Author(s):  
Charles E. Martin ◽  
Kayoko Hiramitsu ◽  
Yasuo Kitajima ◽  
Yoshinori Nozawa ◽  
Lars Skriver ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Membrane Fluidity ◽  
Fatty Acid Desaturase ◽  
Temperature Acclimation ◽  
Membrane Properties ◽  
Molecular Control

scholarly journals Regulation of lipid saturation without sensing membrane fluidity

2019 ◽  
Author(s):  
Stephanie Ballweg ◽  
Erdinc Sezgin ◽  
Dorith Wunnicke ◽  
Inga Hänelt ◽  
Robert Ernst
Keyword(s):  
Membrane Fluidity ◽  
Molecular Mechanisms ◽  
Transmembrane Helix ◽  
Membrane Properties ◽  
Spectroscopic Techniques ◽  
Measured Variable ◽  
Homeoviscous Adaptation ◽  
Acyl Chains ◽  
Single Sensor

Abstract/SummaryCells maintain membrane fluidity by regulating lipid saturation, but the molecular mechanisms of this homeoviscous adaptation remain poorly understood. Here, we have reconstituted the core machinery for sensing and regulating lipid saturation in baker’s yeast to directly characterize its response to defined membrane environments. Using spectroscopic techniques and in vitro ubiquitylation, we uncover a unique sensitivity of the transcriptional regulator Mga2 to the abundance, position, and configuration of double bonds in lipid acyl chains and provide unprecedented insight into the molecular rules of membrane adaptivity. Our data challenge the prevailing hypothesis that membrane viscosity serves as the measured variable for regulating lipid saturation. Rather, we show that the signaling output of Mga2 correlates with the size of a single sensor residue in the transmembrane helix, which senses the lateral pressure and/or compressibility profile in a defined region of the membrane. Our findings suggest that membrane property sensors have evolved remarkable sensitivities to highly specific aspects of membrane structure and dynamics, thus paving the way toward the development of genetically encoded reporters for such membrane properties in the future.

scholarly journals Effect of high levels of CO2 and O2 on membrane fatty acid profile and membrane physiology of meat spoilage bacteria

2021 ◽  
Author(s):  
Sandra Kolbeck ◽  
Hermine Kienberger ◽  
Karin Kleigrewe ◽  
Maik Hilgarth ◽  
Rudi F. Vogel
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Membrane Fluidity ◽  
Fatty Acid Profile ◽  
Membrane Lipid ◽  
Membrane Properties ◽  
Meat Spoilage ◽  
Spoilage Bacteria ◽  
The Impact ◽  
Membrane Physiology

AbstractThe membrane is the major protective barrier separating the cell from the environment and is thus important for bacteria to survive environmental stress. This study investigates changes in membrane lipid compositions and membrane physiology of meat spoiling bacteria in response to high CO2 (30%) and O2 (70%) concentrations, as commonly used for modified atmosphere packaging of meat. Therefore, the fatty acid profile as well as membrane fluidity, permeability and cell surface were determined and correlated to the genomic settings of five meat spoiling bacteria Brochothrix (B.) thermosphacta, Carnobacterium (C.) divergens, C. maltaromaticum, Leuconostoc (L.) gelidum subsp. gelidum and L. gelidum subsp. gasicomitatum cultivated under different gas atmospheres. We identified different genomic potentials for fatty acid adaptations, which were in accordance with actual measured changes in the fatty acid composition for each species in response to CO2 and/or O2, e.g., an increase in saturated, iso and cyclopropane fatty acids. Even though fatty acid changes were species-specific, the general physiological responses were similar, comprising a decreased membrane permeability and fluidity. Thus, we concluded that meat spoiling bacteria facilitate a change in membrane fatty acids upon exposure to O2 and CO2, what leads to alteration of membrane fluidity and permeability. The observed adaptations might contribute to the resistance of meat spoilers against detrimental effects of the gases O2 and CO2 and thus help to explain their ability to grow under different modified atmospheres. Furthermore, this study provides fundamental knowledge regarding the impact of fatty acid changes on important membrane properties of bacteria.

scholarly journals Membrane fluidity is regulated by the C. elegans transmembrane protein FLD-1 and its human homologs TLCD1/2

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Mario Ruiz ◽  
Rakesh Bodhicharla ◽  
Emma Svensk ◽  
Ranjan Devkota ◽  
Kiran Busayavalasa ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Polyunsaturated Fatty Acids ◽  
Membrane Fluidity ◽  
Polyunsaturated Fatty Acid ◽  
Dietary Fatty Acids ◽  
Editorial Note ◽  
Membrane Phospholipids ◽  
C Elegans ◽  
Long Chain

Dietary fatty acids are the main building blocks for cell membranes in animals, and mechanisms must therefore exist that compensate for dietary variations. We isolated C. elegans mutants that improved tolerance to dietary saturated fat in a sensitized genetic background, including eight alleles of the novel gene fld-1 that encodes a homolog of the human TLCD1 and TLCD2 transmembrane proteins. FLD-1 is localized on plasma membranes and acts by limiting the levels of highly membrane-fluidizing long-chain polyunsaturated fatty acid-containing phospholipids. Human TLCD1/2 also regulate membrane fluidity by limiting the levels of polyunsaturated fatty acid-containing membrane phospholipids. FLD-1 and TLCD1/2 do not regulate the synthesis of long-chain polyunsaturated fatty acids but rather limit their incorporation into phospholipids. We conclude that inhibition of FLD-1 or TLCD1/2 prevents lipotoxicity by allowing increased levels of membrane phospholipids that contain fluidizing long-chain polyunsaturated fatty acids.Editorial note: This article has been through an editorial process in which the authors decide how to respond to the issues raised during peer review. The Reviewing Editor's assessment is that all the issues have been addressed (<xref ref-type="decision-letter" rid="SA1">see decision letter</xref>).

Molecular control of membrane properties during temperature acclimation. Membrane fluidity regulation of fatty acid desaturase action?

Biochemistry ◽  
1976 ◽  
Vol 15 (24) ◽  
pp. 5228-5233 ◽  
Author(s):  
Reiko Kasai ◽  
Yasuo Kitajima ◽  
Charles E. Martin ◽  
Yoshinori Nozawa ◽  
Lars Skriver ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Membrane Fluidity ◽  
Fatty Acid Desaturase ◽  
Temperature Acclimation ◽  
Membrane Properties ◽  
Molecular Control

scholarly journals Membrane fluidity adjusts the insertion of the transacylase PlsX to regulate phospholipid biosynthesis in Gram-positive bacteria

2019 ◽  
Vol 295 (7) ◽  
pp. 2136-2147 ◽  
Author(s):  
Diego E. Sastre ◽  
Luis G. M. Basso ◽  
Beatriz Trastoy ◽  
Javier O. Cifuente ◽  
Xabier Contreras ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Membrane Fluidity ◽  
Membrane Insertion ◽  
Phospholipid Biosynthesis ◽  
Membrane Phospholipids ◽  
Gram Positive ◽  
Gram Positive Bacteria ◽  
Acyl Phosphate

PlsX plays a central role in the coordination of fatty acid and phospholipid biosynthesis in Gram-positive bacteria. PlsX is a peripheral membrane acyltransferase that catalyzes the conversion of acyl-ACP to acyl-phosphate, which is in turn utilized by the polytopic membrane acyltransferase PlsY on the pathway of bacterial phospholipid biosynthesis. We have recently studied the interaction between PlsX and membrane phospholipids in vivo and in vitro, and observed that membrane association is necessary for the efficient transfer of acyl-phosphate to PlsY. However, understanding the molecular basis of such a channeling mechanism remains a major challenge. Here, we disentangle the binding and insertion events of the enzyme to the membrane, and the subsequent catalysis. We show that PlsX membrane binding is a process mostly mediated by phospholipid charge, whereas fatty acid saturation and membrane fluidity remarkably influence the membrane insertion step. Strikingly, the PlsXL254E mutant, whose biological functionality was severely compromised in vivo but remains catalytically active in vitro, was able to superficially bind to phospholipid vesicles, nevertheless, it loses the insertion capacity, strongly supporting the importance of membrane insertion in acyl-phosphate delivery. We propose a mechanism in which membrane fluidity governs the insertion of PlsX and thus regulates the biosynthesis of phospholipids in Gram-positive bacteria. This model may be operational in other peripheral membrane proteins with an unprecedented impact in drug discovery/development strategies.

scholarly journals AdipoR1 and AdipoR2 maintain membrane fluidity in most human cell types and independently of adiponectin

2019 ◽  
Vol 60 (5) ◽  
pp. 995-1004 ◽  
Author(s):  
Mario Ruiz ◽  
Marcus Ståhlman ◽  
Jan Borén ◽  
Marc Pilon
Keyword(s):  
Membrane Fluidity ◽  
Human Cell ◽  
Umbilical Vein ◽  
Cell Types ◽  
Hek293 Cells ◽  
Membrane Properties ◽  
Membrane Composition ◽  
Membrane Phospholipids ◽  
Generalized Polarization ◽  
Fa Composition

The FA composition of phospholipids must be tightly regulated to maintain optimal cell membrane properties and compensate for a highly variable supply of dietary FAs. Previous studies have shown that AdipoR2 and its homologue PAQR-2 are important regulators of phospholipid FA composition in HEK293 cells and Caenorhabditiselegans, respectively. Here we show that both AdipoR1 and AdipoR2 are essential for sustaining desaturase expression and high levels of unsaturated FAs in membrane phospholipids of many human cell types, including primary human umbilical vein endothelial cells, and for preventing membrane rigidification in cells challenged with exogenous palmitate, a saturated FA. Three independent methods confirm the role of the AdipoRs as regulators of membrane composition and fluidity: fluorescence recovery after photobleaching, measurements of Laurdan dye generalized polarization, and mass spectrometry to determine the FA composition of phospholipids. Furthermore, we show that the AdipoRs can prevent lipotoxicity in the complete absence of adiponectin, their putative ligand. We propose that the primary cellular function of AdipoR1 and AdipoR2 is to maintain membrane fluidity in most human cell types and that adiponectin is not required for this function.

scholarly journals Menaquinone-mediated regulation of membrane fluidity is relevant for fitness of Listeria monocytogenes

2021 ◽  
Author(s):  
Alexander Flegler ◽  
Vanessa Kombeitz ◽  
André Lipski
Keyword(s):  
Fatty Acid ◽  
Listeria Monocytogenes ◽  
Membrane Fluidity ◽  
Low Temperatures ◽  
Lipid Membrane ◽  
Feedback Inhibition ◽  
Aromatic Amino Acids ◽  
Adaptation Effect ◽  
Membrane Composition ◽  
Lower Growth

AbstractListeria monocytogenes is a food-borne pathogen with the ability to grow at low temperatures down to − 0.4 °C. Maintaining cytoplasmic membrane fluidity by changing the lipid membrane composition is important during growth at low temperatures. In Listeria monocytogenes, the dominant adaptation effect is the fluidization of the membrane by shortening of fatty acid chain length. In some strains, however, an additional response is the increase in menaquinone content during growth at low temperatures. The increase of this neutral lipid leads to fluidization of the membrane and thus represents a mechanism that is complementary to the fatty acid-mediated modification of membrane fluidity. This study demonstrated that the reduction of menaquinone content for Listeria monocytogenes strains resulted in significantly lower resistance to temperature stress and lower growth rates compared to unaffected control cultures after growth at 6 °C. Menaquinone content was reduced by supplementation with aromatic amino acids, which led to a feedback inhibition of the menaquinone synthesis. Menaquinone-reduced Listeria monocytogenes strains showed reduced bacterial cell fitness. This confirmed the adaptive function of menaquinones for growth at low temperatures of this pathogen.

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