Normal DBA/2 mouse cells synthesize a glycoprotein which interferes with MCF virus infection

Bassin, Robert H.; Ruscetti, Sandra K.; Ali, Iqbal Unnisa; Haapala, Daniel K.; Rein, Alan

doi:10.1016/0042-6822(82)90301-4

Cited by 93 publications

(54 citation statements)

References 47 publications

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“…According to the latter explanation, the mask in MDTF might be a retrovirus-related envelope glycoprotein that misfolds in the absence of N-linked glycosylation, but this would not result in tunicamycin-dependent susceptibility to infection because the FLVCR would become inactive in these conditions. This explanation would be compatible with evidence that many but not all glycoproteins misfold in the presence of tunicamycin (2,12,23) and that FLVCR contains three consensus sites for N-linked glycosylation (Fig. 2).…”

supporting

confidence: 71%

Cellular and Species Resistance to Murine Amphotropic, Gibbon Ape, and Feline Subgroup C Leukemia Viruses Is Strongly Influenced by Receptor Expression Levels and by Receptor Masking Mechanisms

Tailor

Nouri

Kabat

2000

J Virol

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Chinese hamster ovary (CHO) cells are resistant to infections by gibbon ape leukemia virus (GALV) and amphotropic murine leukemia virus (A-MLV) unless they are pretreated with tunicamycin, an inhibitor of N-linked glycosylation. These viruses use the related sodium-phosphate symporters Pit1 and Pit2, respectively, as receptors in nonhamster cells, and evidence has suggested that the corresponding transporters of CHO cells may be masked by tunicamycin-sensitive secreted inhibitors. Although the E36 line of Chinese hamster cells was reported to secrete the putative Pit2 inhibitor and to be sensitive to the inhibitory CHO factors, E36 cells are highly susceptible to both GALV and A-MLV in the absence of tunicamycin. Moreover, expression of E36 Pit2 in CHO cells conferred tunicamycin-independent susceptibilities to both viruses. Based on the latter results, it was suggested that E36 Pit2 must functionally differ from the endogenous Pit2 of CHO cells. To test these ideas, we analyzed the receptor properties of CHO Pit1 and Pit2 in CHO cells. Surprisingly, and counterintuitively, transfection of a CHO Pit2 expression vector into CHO cells conferred strong susceptibility to both GALV and A-MLV, and similar overexpression of CHO Pit1 conferred susceptibility to GALV. Thus, CHO Pit2 is a promiscuous functional receptor for both viruses, and CHO Pit1 is a functional receptor for GALV. Similarly, we found that the natural resistance of Mus dunni tail fibroblasts to subgroup C feline leukemia viruses (FeLV-C) was eliminated simply by overexpression of the endogenous FeLV-C receptor homologue. These results demonstrate a novel and simple method to unmask latent retroviral receptor activities that occur in some cells. Specifically, resistances to retroviruses that are caused by subthreshold levels of receptor expression or by stoichiometrically limited masking or interference mechanisms can be efficiently overcome simply by overexpressing the endogenous receptors in the same cells.

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supporting

confidence: 71%

Cellular and Species Resistance to Murine Amphotropic, Gibbon Ape, and Feline Subgroup C Leukemia Viruses Is Strongly Influenced by Receptor Expression Levels and by Receptor Masking Mechanisms

Tailor

Nouri

Kabat

2000

J Virol

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“…Fourth, expression of an SU identical to the Rmcf-encoded Env sequence has been reported only once previously, in a cell line of DBA/2 origin (8). Taken together, these results support previous proposals (1,24) that Rmcf functions by controlling production of a viral Env glycoprotein that interferes with exogenous virus infection.…”

Section: Discussionsupporting

confidence: 81%

Characterization of a Polytropic Murine Leukemia Virus Proviral Sequence Associated with the Virus Resistance GeneRmcfof DBA/2 Mice

Jung

Lyu

Buckler-White

et al. 2002

J Virol

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The DBA/2 mouse Rmcf gene is responsible for in vivo and in vitro resistance to infection by the polytropic mink cell focus-forming (MCF) virus subgroup of murine leukemia viruses (MLVs). Previous studies suggested that Rmcf resistance is mediated by expression of an interfering MCF MLV envelope (Env) gene. To characterize this env gene, we examined resistance in crosses between Rmcf r DBA/2 mice and Mus castaneus, a species that lacks endogenous MCF env sequences. In backcross progeny, inheritance of Rmcf resistance correlated with inheritance of a specific endogenous MCF virus env-containing 4.6-kb EcoRI fragment. This fragment was present in the DBA/2N substrain with Rmcf-mediated resistance but not in virus-susceptible DBA/2J substrain mice. This fragment contains a provirus with a 5 long terminal repeat and the 5 half of env; the gag and pol genes have been partially deleted. The Env sequence is identical to that of a highly immunogenic viral glycoprotein expressed in the DBA/2 cell line L5178Y and closely resembles the env genes of modified polytropic proviruses. The coding sequence for the full-length Rmcf Env surface subunit was amplified from DNAs from virus-resistant backcross mice and was cloned into an expression vector. NIH 3T3 and BALB 3T3 cells stably transfected with this construct showed significant resistance to infection by MCF MLV but not by amphotropic MLV. This study identifies an Rmcf-linked MCF provirus and indicates that, like the ecotropic virus resistance gene Fv4, Rmcf may mediate resistance through an interference mechanism.

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“…Molecularly cloned amphotropic virus 4070A (19,20) was propagated in NIH 3T3 cells in DMEM containing 10% FCS. The titer of the infectious virus in stocks from the medium of infected cells was determined in an assay by using PG-4 cat cell line (21). Briefly, PG-4 cells were infected with serial dilutions of virus in the presence of 8 g͞ml polybrene.…”

Section: Methodsmentioning

confidence: 99%

Identification of genes that synergize with Cbfb-MYH11 in the pathogenesis of acute myeloid leukemia

Castilla

Perrat

Martínez

et al. 2004

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

117

110

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Acute myeloid leukemia subtype M4 with eosinophilia is associated with a chromosome 16 inversion that creates a fusion gene CBFB-MYH11. We have previously shown that CBFB-MYH11 is necessary but not sufficient for leukemogenesis. Here, we report the identification of genes that specifically cooperate with CBFB-MYH11 in leukemogenesis. Neonatal injection of Cbfb-MYH11 knock-in chimeric mice with retrovirus 4070A led to the development of acute myeloid leukemia in 2-5 months. Each leukemia sample contained one or a few viral insertions, suggesting that alteration of one gene could be sufficient to synergize with Cbfb-MYH11. The chromosomal position of 67 independent retroviral insertion sites (RISs) was determined, and 90% of the RISs mapped within 10 kb of a flanking gene. In total, 54 candidate genes were identified; six of them were common insertion sites (CISs). CIS genes included members of a zinc finger transcription factors family, Plag1 and Plagl2, with eight and two independent insertions, respectively. CIS genes also included Runx2, Myb, H2-T24, and D6Mm5e. Comparison of the remaining 48 genes with single insertion sites with known leukemia-associated RISs indicated that 18 coincide with known RISs. To our knowledge, this retroviral genetic screen is the first to identify genes that cooperate with a fusion gene important for human myeloid leukemia.

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Normal DBA/2 mouse cells synthesize a glycoprotein which interferes with MCF virus infection

Cited by 93 publications

References 47 publications

Cellular and Species Resistance to Murine Amphotropic, Gibbon Ape, and Feline Subgroup C Leukemia Viruses Is Strongly Influenced by Receptor Expression Levels and by Receptor Masking Mechanisms

Cellular and Species Resistance to Murine Amphotropic, Gibbon Ape, and Feline Subgroup C Leukemia Viruses Is Strongly Influenced by Receptor Expression Levels and by Receptor Masking Mechanisms

Characterization of a Polytropic Murine Leukemia Virus Proviral Sequence Associated with the Virus Resistance GeneRmcfof DBA/2 Mice

Identification of genes that synergize with Cbfb-MYH11 in the pathogenesis of acute myeloid leukemia

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