Induction of membrane fusion by polysialogangliosides

Maggio, Bruno; Cumar, Federico A.; Caputto, Ranwel

doi:10.1016/0014-5793(78)80318-4

Cited by 50 publications

(19 citation statements)

References 10 publications

(17 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This interaction of Sendai virus with gangliosides such as GDla, GTla, and GQ1b on the cell surface suggests a possible mechanism for inducing the ensuing virus-cell fusion. Polysialogangliosides such as GDla and GT1 have been shown to induce cell-cell fusion when incubated with cells for 2-3.5 hr (32). It is possible that the attachment of a highly multivalent ligand such as Sendai virus (12) to the cell surface may temporarily stabilize a clustering of its receptors, the polysialogangliosides GDla, GTMb, and GQlb, in the very region of the host membrane where virus-cell fusion should occur.…”

Section: Methodsmentioning

confidence: 99%

Specific gangliosides function as host cell receptors for Sendai virus.

Markwell¹,

Svennerholm²,

Paulson³

1981

Proc. Natl. Acad. Sci. U.S.A.

242

104

View full text Add to dashboard Cite

The ability of specific gangliosides to function as host cell receptors for Sendai virus was investigated by using Madin-Darby bovine kidney cells which become resistant to infection upon treatment with Vibrio cholerae sialidase. Sialidase-treated cells were incubated for 20 min at 37 degrees C with individual, highly purified gangliosides containing homogeneous carbohydrate moieties and then inoculated with virus for 10 min. Susceptibility of the cells to infection was monitored by hemagglutination titer of the virus produced 48 hr after inoculation. Incubation of the cells with gangliosides containing the sequence NeuAc alpha 2,3Gal beta 1,3GalNAc (i.e., GD1a, GT1b, and GQ1b) fully restored susceptibility to infection to the cells. However, the ganglioside GQ1b in which the sequence ends with two sialic acids in a NeuAc alpha 2,8NeuAc linkage instead of a single sialic acid as in GD1a and GT1b, was effective as a receptor at a concentration 1/100th that of any of the other gangliosides tested. Incubation with gangliosides similar in structure to GD1a, GT1b, and GQ1b but lacking the sialic acid attached to the terminal galactose (i.e., GM1 and GD1b) had no effect. The results from control experiments in which gangliosides were incubated at 0 degrees C with cells or in which trypsin was used to remove gangliosides adsorbed to cells were consistent with the premise that the gangliosides must actually insert into the cellular membrane to function as Sendai virus receptors. Addition of 4 X 10(6) molecules of 14C-labeled GD1a per cell made the cells fully susceptible to infection. Analysis of the ganglioside content of cell membranes showed that gangliosides GD1a, GT1b, and GQ1b are natural components of these cells and are present in quantities sufficient to act as receptors. These results demonstrate that gangliosides with the proper carbohydrate sequence, such as GD1a, GT1b, and GQ1b, function as natural receptors for Sendai virus in host cells.

show abstract

Section: Methodsmentioning

confidence: 99%

Specific gangliosides function as host cell receptors for Sendai virus.

Markwell¹,

Svennerholm²,

Paulson³

1981

Proc. Natl. Acad. Sci. U.S.A.

242

104

View full text Add to dashboard Cite

show abstract

“…In this context, SM appears to modulate the transbilayer distribution of GalCer [125,126], while sphingomyelinase conversion of SM to Cer on the external leaflet of bilayer vesicles promotes transbilayer movement of ganglioside GM3 [127]. Sphingolipids were early implicated in regulating processes of membrane fusion [6,7,68,71] and separation of the ability to fuse from efficiency of the process suggested a dependence on microdomain organization and it was proposed that the generation of Cer by sphingomyelinase may preserve the membrane ability to fuse by contributing to the total membrane negative curvature [128].…”

Section: Intermolecular Packing Incompatibility Of Sphingoand Glycospmentioning

confidence: 98%

“…Besides, H II -phase like regions act as key structural intermediates for inducing cell and lipid bilayer membrane fusion or fission [153]. These effects correlate with the capacity of several sphingolipids to affect hemi-fusion, whole bilayer vesicle fusion, fusionmediated exocytotic neurotransmitter release, and whole cell fusion depending on their relative proportions and the type of polar head group [67,68,70,71,154]. Recent studies showed the importance of mutual thermodynamicgeometric compensations and lateral condensation among sphingolipids with different local geometries for the adoption of self-assembled structure of defined curvature, depending on their relative proportions [90].…”

Section: Interfacial Thickness Curvature and Topological Rearrangementmentioning

confidence: 98%

“…On the other hand, hydrated gangliosides and Gal-sphingosine (psychosine) form oil-in-water (H I type) mesophases [64][65][66]. Through this type of interplay among structural distortions and surface tensions GSLs can affect the H IIphase-mediated lipid bilayer and cell membrane fusion [67][68][69][70][71]. The behavior of ''non-sphingo'' glycolipids that are major constituents of plant, bacteria and mycoplasma membranes also indicates the influence of the carbohydrate moiety in the polar head group on the structural toplogy (for references, see [72][73][74].…”

Section: Sphingolipid-induced Isothermal Phase Domain Segregationmentioning

confidence: 99%

See 1 more Smart Citation

Composition-driven Surface Domain Structuring Mediated by Sphingolipids and Membrane-active Proteins

Maggio

Borioli

Boca

et al. 2007

Cell Biochem Biophys

Self Cite

View full text Add to dashboard Cite

Biomembranes contain a wide variety of lipids and proteins within an essentially two-dimensional structure. The coexistence of such a large number of molecular species causes local tensions that frequently relax into a phase or compositional immiscibility along the lateral and transverse planes of the interface. As a consequence, a substantial microheterogeneity of the surface topography develops and that depends not only on the lipid-protein composition, but also on the lateral and transverse tensions generated as a consequence of molecular interactions. The presence of proteins, and immiscibility among lipids, constitute major perturbing factors for the membrane sculpturing both in terms of its surface topography and dynamics. In this work, we will summarize some recent evidences for the involvement of membrane-associated, both extrinsic and amphitropic, proteins as well as membrane-active phosphohydrolytic enzymes and sphingolipids in driving lateral segregation of phase domains thus determining long-range surface topography.

show abstract

“…The molecular mechanisms of the protein-induced fusion probably include modifications of the membrane organization and molecular rearrangements that cause transient destabilization of the bilayers [5,6]. It has been reported that sulfatides have special interactions with choline-containing phospholipids, characterized by reduction of molecular packing in monolayers [7] and formation of unstable domains within the phospholipid bilayers of the type which have been described for several lipids capable of inducing membrane fusion [S]. In this work, we have used phosphatidylcholine vesicles containing sulfatides as a model to study induced fusion.…”

mentioning

confidence: 99%

Fusion of Sulfatide‐Containing Vesicles of Phosphatidylcholine

Cestaro

Cervato

Barenghi

et al. 1983

European Journal of Biochemistry

View full text Add to dashboard Cite

Positively charged albumin is described as a 'useful tool' to induce both aggregation and fusion of phosphatidylcholine vesicles containing sulfatide. Techniques that include light-scattering, Sepharose chromatography, centrifugation, electron microscopy, trapped volume determination and scanning calorimetry demonstrate that extensive fusion occurs during aggregation when sulfatide concentrations are above 4 -5 mol"/,. The rate of fusion increases with time for 1 -2 h, then reaches a plateau. Fusion occurs extensively above the transition temperature of the phospholipid and is strongly inhibited by increasing concentration of vesicle cholesterol. The significance of both membrane fluidity and sulfatide-phospholipid organization in the fusion mechanism are discussed.Fusion between membranes is an important step in many cellular processes such as secretion, endocytosis and mitosis.Small unilamellar vesicles are one basic model system which has been employed to investigate membrane fusion at the molecular level. The potential role of proteins in membrane fusion has been repeatedly stressed. Recently, soluble proteins and peptides have indeed been shown to induce aggregation and fusion in vesicle systems [I -41. The molecular mechanisms of the protein-induced fusion probably include modifications of the membrane organization and molecular rearrangements that cause transient destabilization of the bilayers [5,6]. It has been reported that sulfatides have special interactions with choline-containing phospholipids, characterized by reduction of molecular packing in monolayers [7] and formation of unstable domains within the phospholipid bilayers of the type which have been described for several lipids capable of inducing membrane fusion [S]. In this work, we have used phosphatidylcholine vesicles containing sulfatides as a model to study induced fusion. Serum albumin, a well characterized soluble protein, has been found to be a useful tool for inducing vesicle aggregation and detecting the fusion-stimulating activity of sulfatide. In our albumin-vesicle system, techniques including light-scattering, Sepharose chromatography, centrifugation, electron microscopy, trapped volume measurement and scanning calorimetry were made to follow both the aggregation and fusion of vesicles allowing separation of these phenomena into distinct steps. MATERIALS AND METHODSAnalytical grade chemicals, distilled solvents and doubly distilled water were used. Cholesterol, dipalmitoylglycerophosphocholine, dimyristoylglycerophosphocholine, egg phosphatidylcholine and bovine serum albumin (fatty-acid-free) were purchased from Sigma Chemical. Co. ; Sepharose CL2B and Sephadex G-25 from Pharmacia; ~>-['~C]glucose from Amersham, and liquid scintillation counting mixture (Instagel) from Packard.Ceramide galactose 3-sulfate ('sulfatide') was obtained from Supelco. It was further purified chromatographically and converted to the sodium salt as previously described [9]. Preparation of Small Unilamellar VesiclesSmall unilamellar vesicles of phosphati...

show abstract

Induction of membrane fusion by polysialogangliosides

Cited by 50 publications

References 10 publications

Specific gangliosides function as host cell receptors for Sendai virus.

Specific gangliosides function as host cell receptors for Sendai virus.

Composition-driven Surface Domain Structuring Mediated by Sphingolipids and Membrane-active Proteins

Fusion of Sulfatide‐Containing Vesicles of Phosphatidylcholine

Contact Info

Product

Resources

About