Binding specificities of the lectins from <i>Helix pomatia</i>, soybean and peanut against different glycosphingolipids in liposome membranes

Månsson, Jan‐Eric; Olofsson, Sigvard

doi:10.1016/0014-5793(83)80506-7

Cited by 20 publications

(11 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…WGA is a lectin that has high affinity for N-acetylglucosamine and N-acetylneuraminic acid moieties present on surface proteins (30) and is efficiently endocytosed (5,10,42). It has been shown that most WGA inoculated intramuscularly (into the flexor forelimb muscle) is transported retrogradely to the motor neuron cell bodies located in the ventral horn of the spinal cord in mice (4).…”

Section: Resultsmentioning

confidence: 99%

Receptor-Dependent and -Independent Axonal Retrograde Transport of Poliovirus in Motor Neurons

Ohka

Sakai

Bohnert

et al. 2009

J Virol

View full text Add to dashboard Cite

Poliovirus (PV), when injected intramuscularly into the calf, is incorporated into the sciatic nerve and causes an initial paralysis of the inoculated limb in transgenic (Tg) mice carrying the human PV receptor (hPVR/ CD155) gene. We have previously demonstrated that a fast retrograde axonal transport process is required for PV dissemination through the sciatic nerves of hPVR-Tg mice and that intramuscularly inoculated PV causes paralytic disease in an hPVR-dependent manner. Here we showed that hPVR-independent axonal transport of PV was observed in hPVR-Tg and non-Tg mice, indicating that several different pathways for PV axonal transport exist in these mice. Using primary motor neurons (MNs) isolated from these mice or rats, we demonstrated that the axonal transport of PV requires several kinetically different motor machineries and that fast transport relies on a system involving cytoplasmic dynein. Unexpectedly, the hPVR-independent axonal transport of PV was not observed in cultured MNs. Thus, PV transport machineries in cultured MNs and in vivo differ in their hPVR requirements. These results suggest that the axonal trafficking of PV is carried out by several distinct pathways and that MNs in culture and in the sciatic nerve in situ are intrinsically different in the uptake and axonal transport of PV.In humans, paralytic poliomyelitis results from the invasion of the central nervous system by circulating poliovirus (PV), probably via the blood-brain barrier. This conclusion is supported by the finding that circulating PV after intravenous inoculation in mice appears to cross the blood-brain barrier at a high rate in a human PV receptor (hPVR/CD155)-independent manner (44). After the virus enters the central nervous system, it replicates in neurons, especially in motor neurons (MNs), inducing the cell death that causes paralytic poliomyelitis. Along with this route of dissemination, a neuron-specific pathway has been reported in humans (31), monkeys (18), and PV-sensitive transgenic (Tg) mice carrying the hPVR gene (34,37). This neuron-specific pathway appears to be important in causing "provocation poliomyelitis," which is triggered by injuries after PV ingestion (11). Using differentiated PC12 cells and a PV-sensitive Tg mouse line, we have shown that intramuscularly inoculated PV is taken up by endocytosis at synapses.hPVR is a member of the immunoglobulin (Ig) superfamily, with three linked extracellular Ig-like domains, followed by a membrane-spanning domain and a cytoplasmic domain. Two membrane-bound forms (␣ and ␦) and two secreted forms (␤ and ␥) of hPVR derived by alternative splicing are likely to be expressed in human cells (23). Membrane-bound hPVRs are considered to play important roles in the early steps of infection, such as the binding of the virus to the cell surface, its entry into the cell, and the uncoating of the virus. The N-terminal Ig-like domain harbors the sites for PV binding, and antihPVR monoclonal antibodies (MAbs) directed against this region block PV infection (9,24,39).hPVR ...

show abstract

Section: Resultsmentioning

confidence: 99%

Receptor-Dependent and -Independent Axonal Retrograde Transport of Poliovirus in Motor Neurons

Ohka

Sakai

Bohnert

et al. 2009

J Virol

View full text Add to dashboard Cite

show abstract

“…WGA, the lectin used in the present study, binds to sialic acid when the acid is present at certain specific positions of the oligosaccharide (M~nsson & Olofsson, 1983). When the effects of three compounds (taxol, nocodazole and EHNA) on the neuritic transport of WGA and HSV in rat sensory neurons were compared, all three were found to have an equal blocking capacity in the lectin and the virus systems.…”

mentioning

confidence: 89%

Neuritic Transport of Herpes Simplex Virus in Rat Sensory Neurons in vitro. Effects of Substances Interacting with Microtubular Function and Axonal Flow [Nocodazole, Taxol and Erythro-9-3-(2-hydroxynonyl)adenine]

Kristensson

Lycke²,

Röyttä

et al. 1986

Journal of General Virology

117

View full text Add to dashboard Cite

SUMMARYHerpes simplex virus type 1 and a fluorescein-labelled lectin (wheat germ agglutinin) were selectively transported to nerve cell bodies located in the inner compartment of a two-chamber tissue culture system after the application of virus or lectin to the neuritic processes in the outer culture compartment. Taxol, which stabilizes and alters intracellular arrangements of microtubules, and nocodazole, which disrupts microtubules, both inhibited this retrograde axonal transport of viral particles and lectin. The transport was also inhibited by erythro-9-3-(2-hydroxynonyl)adenine (EHNA), which blocks ATPases. However, EHNA was also an effective inhibitor of infection with the virus in non-neuronal cells (GMK AH-1). The nature of the action(s) of EHNA on neuritic transport of the virus is therefore less clear.The pathogenesis of herpes simplex virus (HSV) infections involves axonal transport of virus and viral subunits by sensory neurons in the anterograde as well as the retrograde direction. Neurites of dissociated dorsal root ganglion cells have the capacity to internalize the virus (Ziegler & Herman, 1980), presumably by fusion of the viral envelope with the neuritic plasma membrane (Lycke et al., 1984). Since nucleocapsids are detectable in neurites exposed to HSV and are seen around nuclear pores in HSV-infected cell lines (Batterson et al., 1983), we assume that they are involved in retrograde axonal transport of the virus. The mechanisms of this axonal transport of HSV remain to be clarified.We now report the effects on neuritic transport of HSV of three substances capable of inhibiting intracellular transport of endosomes, namely nocodazole, which causes disruption of microtubules, and taxol, which promotes assembly of microtubules (Herman & Albertini, 1984); the third drug, erythro-9-3-(2-hydroxynonyl)adenine (EHNA) (Bouchard et al., 1981) is supposed to inhibit the function of the microtubule-associated ATPase dynein and can inhibit the retrograde movement of organelles in axons. EHNA is considered to have less effect on anterograde axonal transport (Forman et al., 1983).We have used a two-chamber culture system allowing us to infect the neuritic extensions of rat sensory neurons cultured in vitro, without exposing the cell bodies to the virus. For evaluation of the results the neuritic transfer of HSV was compared with the transport of wheat germ agglutinin (WGA).The two-chamber system employed has been described previously (Ziegler & Herman, 1980). Briefly, 35 mm collagen-coated plates were scratched on the bottom, fitted in the centre with an 8 mm cloning cylinder kept in place by silicone high vacuum grease and seeded in the cloning cylinder with trypsin-dissociated dorsal root ganglion (DRG) cells. The cells were obtained by dissecting eight to ten embryos of 16 to 17 day pregnant Sprague-Dawley rats. Trypsinization was performed for 30 min at 37 °C using 0.25~ trypsin (porcine pancreas, type 2, Sigma) in a Ca z÷-and MgZ+-free Hanks' buffer pH 7.2. For the first 2 days, the cells were cultured ...

show abstract

“…The glycopeptides in the Vt peak most probably contained O-linked oligosaccharides because of their small Mr and because they contained a large amount of GaIN (data not shown). Three lectins (HPA, PNA and WGA) were used: HPA is specific for terminal N-acetylgalactosamine (Hammarstrom et al, 1977;Goldstein & Hayes, 1978); PNA has a narrow specificity for the terminal disaccharide sequence GaI(1-3)GalNAc (Goldstein & Hayes, 1978, Mansson & Olofsson, 1983; WGA has affinity for non-reducing terminal sialic acid and GlcNAc residues (Peters et al, 1979). Analysis of gC-II glycopeptides from SF or U-373MG cells showed that they have very little affinity for HPA lectin ( Fig.…”

Section: Lectin Analysis Of Vt Peak Obtained From Infected U-373mg Anmentioning

confidence: 99%

Processing of human cytomegalovirus envelope glycoproteins in and egress of cytomegalovirus from human astrocytoma cells

Kari

Radeke²,

Gehrz³

1992

Journal of General Virology

View full text Add to dashboard Cite

The synthesis of human cytomegalovirus (HCMV) envelope glycoproteins and the production of infectious HCMV in human astrocytoma and skin fibroblast (SF) cells were analysed. HCMV envelope glycoproteins synthesized in astrocytoma cells had lower Mrs than the same glycoproteins synthesized in SF cells regardless of the strain of HCMV used, showing that the differences observed were due to differences in processing by the host cell and not the strain of HCMV used. HCMV envelope glycoproteins synthesized in astrocytoma cells were found to contain less galactosamine. Moreover, when synthesized in SF cells some HCMV glycoproteins contained a protease-resistant fragment owing to the presence of a cluster of O-linked oligosaccharides on the polypeptide. This fragment was not present when these HCMV glycoproteins were synthesized in astrocytoma cells. These data suggested that HCMV glycoproteins synthesized in astrocytoma cells contain fewer O-linked oligosaccharides. In contrast, other post-translational events such as proteolytic cleavage of the HCMV gB glycoprotein and the formation of disulphide-linked complexes did occur. The virus produced in astrocytoma ceils was capable of infecting SF cells, suggesting that complete O-glycosylation is not needed to produce infectious HCMV. However, astrocytoma cells were slow to release virus into the culture medium, suggesting that a fully functional Golgi network is needed for efficient egress of HCMV from the host cell.

show abstract

Binding specificities of the lectins from Helix pomatia, soybean and peanut against different glycosphingolipids in liposome membranes

Cited by 20 publications

References 17 publications

Receptor-Dependent and -Independent Axonal Retrograde Transport of Poliovirus in Motor Neurons

Receptor-Dependent and -Independent Axonal Retrograde Transport of Poliovirus in Motor Neurons

Neuritic Transport of Herpes Simplex Virus in Rat Sensory Neurons in vitro. Effects of Substances Interacting with Microtubular Function and Axonal Flow [Nocodazole, Taxol and Erythro-9-3-(2-hydroxynonyl)adenine]

Processing of human cytomegalovirus envelope glycoproteins in and egress of cytomegalovirus from human astrocytoma cells

Contact Info

Product

Resources

About