Fusion of SV40-induced endocytotic vacuoles with the nuclear membrane.

Nishimura, Toshikazu; Kawai, Norio; Kikuchi, Makoto; Notake, Kunihiro; Ichihara, Ichiro

doi:10.1247/csf.11.135

Cited by 23 publications

(15 citation statements)

References 24 publications

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“…Papovaviruses are reported to be uncoated in the nucleus (2,14), and workers in several laboratories have reported that lysosomotropic agents have no effect on SV40 entry (24,29,33). Papovavirus-containing vesicles have been reported to be transported to the nucleus, where they are thought to fuse with the outer nuclear membrane, delivering virus particles into the perinuclear cisternae (9,11,20,23). It has been reported that plasma membrane markers are transported to the outer nuclear membrane in SV40-or polyoma-infected cells but not in control cells; therefore, this vesicular transport pathway may be unique to papovaviruses (9,23).…”

Section: Discussionmentioning

confidence: 99%

“…Papovavirus-containing vesicles have been reported to be transported to the nucleus, where they are thought to fuse with the outer nuclear membrane, delivering virus particles into the perinuclear cisternae (9,11,20,23). It has been reported that plasma membrane markers are transported to the outer nuclear membrane in SV40-or polyoma-infected cells but not in control cells; therefore, this vesicular transport pathway may be unique to papovaviruses (9,23). All the viruses which have been previously reported to enter cells in a polarized manner (vesicular stomatitis virus [7], Semliki Forest virus [8], and reovirus types 1 and 2 [27] exclusively from the basolateral surface.…”

Section: Discussionmentioning

confidence: 99%

“…These virion-containing vesicles are reported to be transported directly to the nucleus and to fuse with the outer nuclear membrane (11,20,23). The virus is then thought to be transported across the inner nuclear membrane (by an unknown mechanism) into the nucleoplasm, where virus uncoating and virus replication occur (2).…”

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Entry of simian virus 40 is restricted to apical surfaces of polarized epithelial cells.

Clayson¹,

Compans²

1988

Mol. Cell. Biol.

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The uptake of simian virus 40 (SV40) by polarized epithelial cells was investigated by growth of cells on permeable supports and inoculation on either the apical or the basolateral surface. Binding of radiolabeled SV40 occurred on the apical but not the basolateral surfaces of permissive polarized Vero Polarized epithelial cells are characterized by the presence of two plasma membrane domains: the apical domain, which lines the epithelial lumen, and the basolateral domain, which faces underlying tissues in vivo. These two domains are separated by a continuous belt of tight junctional complexes which maintain the unique protein and lipid compositions of each domain (30). Certain enveloped viruses have been shown to enter polarized epithelial cells preferentially from the basolateral domain (7,8). The polarity of viral entry is presumed to be the result of the polarized expression of viral receptors. The entry of a virus exclusively from the apical surface has not been previously reported. We have recently shown that simian virus 40 (SV40), a nonenveloped virus, is released preferentially from the apical surface of polarized epithelial cells (Clayson et al., submitted for publication), and we have investigated the entry of SV40 in the present study.SV40 adsorbs to the cell surface, where it is internalized either individually or in small groups in endocytic vesicles. These virion-containing vesicles are reported to be transported directly to the nucleus and to fuse with the outer nuclear membrane (11,20,23). The virus is then thought to be transported across the inner nuclear membrane (by an unknown mechanism) into the nucleoplasm, where virus uncoating and virus replication occur (2). In order to determine whether the binding of SV40 is polarized in permissive cells grown on permeable supports, an assay for the binding of radiolabeled SV40 virions to cell monolayers was developed. Electron microscopy was also used to demonstrate virus binding to cell surfaces. Productive infection of cells infected from either apical or basolateral surfaces was determined by plaque assay of the progeny virus produced, and viral capsid protein synthesis in cells infected from either apical or basolateral surfaces was analyzed by indirect immunofluorescence. * Corresponding author. MATERIALS AND METHODSCells and virus. Polarized Vero C1008, CV-1, and primary African green monkey kidney (AGMK) cells were obtained and grown as previously described (Clayson et al., submitted). Nonpolarized Vero and polarized Madin-Darby canine kidney (MDCK) cells were purchased from the American Type Culture Collection and were maintained in Dulbecco modified Eagle medium supplemented with 10% newborn calf serum. Purified canine parvovirus was a gift from Sukla Basak. SV40 stocks were prepared and titers were determined as previously described (Clayson et al., submitted). For preparation of purified 3H-labeled SV40 virus, infected monolayers were incubated in leucine-free Eagle medium supplemented with 2% fetal bovine serum and 10 ,uCi of L-[4,5-3H]...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Entry of simian virus 40 is restricted to apical surfaces of polarized epithelial cells.

Clayson¹,

Compans²

1988

Mol. Cell. Biol.

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“…Early work with the mouse polyomavirus and simian virus 40 (SV40) demonstrated that these virions were internalized into monopinocytotic vesicles which then accumulated at the nuclear membrane (12, 16). In some studies, viral particles were also seen in the nucleus, suggesting that the nucleus was the site of uncoating (7,19,21). More recent studies have shown that SV40 enters cells by receptor-mediated endocytosis into uncoated membrane-bound invaginations known as caveolae (1,2,24).…”

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confidence: 99%

JC Virus Enters Human Glial Cells by Clathrin-Dependent Receptor-Mediated Endocytosis

Pho

Ashok

Atwood

2000

J Virol

225

190

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The human polyomavirus JC virus (JCV) is the etiologic agent of a fatal central nervous system (CNS) demyelinating disease known as progressive multifocal leukoencephalopathy (PML). PML occurs predominantly in immunosuppressed patients and has increased dramatically as a result of the AIDS pandemic. The major target cell of JCV infection and lytic replication in the CNS is the oligodendrocyte. The mechanisms by which JCV initiates and establishes infection of these glial cells are not understood. The initial interaction between JCV and glial cells involves virus binding to N-linked glycoproteins containing terminal ␣(2-6)-linked sialic acids. The subsequent steps of entry and targeting of the viral genome to the nucleus have not been described. In this report, we compare the kinetics and mechanisms of infectious entry of JCV into human glial cells with that of the related polyomavirus, simian virus 40 (SV40). We demonstrate that JCV, unlike SV40, enters glial cells by receptor-mediated clathrin-dependent endocytosis.JC virus (JCV) is a small, nonenveloped, double-stranded DNA containing virus belonging to the family Papovaviridae and the subfamily Polyomavirinae (23, 26). In vivo, JCV infection is restricted to oligodendrocytes, astrocytes, and B lymphocytes (17,20). This highly restricted cell type specificity is also seen in vitro, as JCV infects primary cultures of human glial cells, human glial cell lines, and to a limited extent, primary human B cells and some B-cell lines (4,17,20,28). The life cycle of JCV begins with virus attachment to a cell surface glycoprotein receptor containing ␣-(2-6)-linked sialic acid (15). Following attachment, the JCV virion must penetrate the plasma membrane and target its genome to the nucleus. Very little is known about the mechanisms of polyomavirus entry and nuclear targeting. Early work with the mouse polyomavirus and simian virus 40 (SV40) demonstrated that these virions were internalized into monopinocytotic vesicles which then accumulated at the nuclear membrane (12, 16). In some studies, viral particles were also seen in the nucleus, suggesting that the nucleus was the site of uncoating (7,19,21). More recent studies have shown that SV40 enters cells by receptor-mediated endocytosis into uncoated membrane-bound invaginations known as caveolae (1,2,24). An interaction between SV40 and major histocompatibility complex-encoded class I proteins induces the clustering of virus-receptor complexes into caveolin-rich membrane domains (5,8,24). Intracellular signals induced by SV40 binding to cells result in increased caveola-dependent endocytosis of the virus and delivery of the virions to the endoplasmic reticulum (9, 24). It is unclear how the viral genome is then targeted from the endoplasmic reticulum to the nucleus.In this report, we studied the kinetics of JCV and SV40 infectious entry into human glial cells. Our results demonstrate that JCV rapidly enters glial cells and is completely internalized into a neutralizing antibody-resistant compartment within 30 min. SV40 ...

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“…This includes well-developed junction complexes between cells, abundant microvilli, and primary cilia. In addition, these cells lack the vacuoles and lysosomal compartments that are often found in oncogene-transformed cells (26,27). The mTERT-CCD cells also exhibit Na ϩ transport via ENaC, as assessed using patch clamp and whole cell conductance.…”

Section: Discussionmentioning

confidence: 99%

Telomerase immortalization of principal cells from mouse collecting duct

Steele¹,

Kolb

et al. 2010

American Journal of Physiology-Renal Physiology

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Recently, the use of overexpression of telomerase reverse transcriptase (TERT) has led to the generation of immortalized human cell lines. However, this cell immortalization approach has not been reported in well-differentiated mouse cells, such as renal epithelial cells. We sought to establish and then characterize a mouse collecting duct cell line, using ectopic expression of mTERT. Isolated primary cortical collecting duct (CCD) cell lines were transduced with mouse (m)TERT, using a lentiviral vector. mTERT-negative cells did not survive blasticidin selection, whereas mTERT-immortalized cells proliferated in selection media for over 40 subpassages. mTERT messenger RNA and telomerase activity was elevated in these cells, compared with an SV40-immortalized cell line. Flow cytometry with Dolichos biflorus agglutinin was used to select the CCD principal cells, and we designated this cell line mTERT-CCD. Cells were well differentiated and exhibited morphological characteristics typically found in renal epithelial cells, such as tight junction formation, microvilli, and primary cilia. Further characterization using standard immunofluorescence revealed abundant expression of aquaporin-2 and the vasopressin type 2 receptor. mTERT-CCD cells exhibited cAMP-stimulated/benzamil-inhibited whole cell currents. Whole cell patch-clamp currents were also enhanced after a 6-day treatment with aldosterone. In conclusion, we have successfully used mTERT to immortalize mouse collecting duct cells that retain the basic in vivo phenotypic characteristics of collecting duct cells. This technique should be valuable in generating cell lines from genetically engineered mouse models.

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Fusion of SV40-induced endocytotic vacuoles with the nuclear membrane.

Cited by 23 publications

References 24 publications

Entry of simian virus 40 is restricted to apical surfaces of polarized epithelial cells.

Entry of simian virus 40 is restricted to apical surfaces of polarized epithelial cells.

JC Virus Enters Human Glial Cells by Clathrin-Dependent Receptor-Mediated Endocytosis

Telomerase immortalization of principal cells from mouse collecting duct

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