The dependence of erythroid differentiation on cell replication in dimethyl sulfoxide-treated friend leukemia-virus-infected cells

The process of erythroid differentiation in mouse Friend leukemia virus transformed cells (T3-C1-2) was examined by following changes in several enzyme activities of the heme biosynthetic pathway and in heme concentration while the cells were undergoing erythroid differentiation after treatment with dimethylsulfoxide. Untreated cells on the one hand, have a limited capacity for spontaneous differentiation. On the other hand, dimethylsulfoxide(DMSO)-treated cells showed an increase in the activities of delta-aminolevulinic acid (ALA) synthetase, ALA dehydratase, uroporphyrinogen-I synthetase, ferrochelatase, and heme concentration by days 1, 1.5, 2, and 4, respectively. The increase of the heme pathway enzymes and heme concentration followed the order of these enzymes or products as they are arranged in the heme biosynthetic pathway. These changes induced by DMSO were effectively inhibited by treatment with actinomycin D, suggesting that continued RNA synthesis is required for the differentiation process. 5-bromo-2'-deoxyuridine (BrdU) (10(-5) M) inhibited the DMSO-induced changes of the heme pathway enzymes. BrdU was most effective when it was present during the first 2 days of cell culture. It gradually lost its inhibitory effect when added after the 3rd day or later. The BrdU-mediated inhibition was completely overcome by the addition of thymidine (7 x 10(-5) M), but not by uridine (7 x 10(-5) M). All these data suggest that a sequential induction of the heme pathway enzyme takes place during erythroid differentiation of Friend leukemia cells, and that the sequential induction of the enzymes may be due to a sequential activation of genes coding for these enzyme activities.

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EVIDENCE FOR TRANSFORMATION OF SPLEEN CELLS ONE DAY AFTER INFECTION OF MICE WITH FRIEND LEUKEMIA VIRUS

Journal of Experimental Medicine ◽

10.1084/jem.131.4.765 ◽

1970 ◽

Vol 131 (4) ◽

pp. 765-781 ◽

Cited By ~ 15

Author(s):

Giovanni B. Rossi ◽

Gustavo Cudkowicz ◽

Charlotte Friend

Keyword(s):

Leukemia Virus ◽

Erythroid Differentiation ◽

Growth Potential ◽

Leukemic Cells ◽

F1 Hybrid ◽

Hemopoietic Cells ◽

Friend Leukemia ◽

Friend Leukemia Virus ◽

Marrow Cells

Proliferation and erythroid differentiation of transplanted DBA/2 marrow cells and Friend virus-induced leukemic cells were assessed in syngeneic, allogeneic (H-2 compatible), and (BALB/c x DBA/2)F1 hybrid mice (CDF1). Measurements were made 5 days after transplantation of donor cells into nonirradiated or X-irradiated mice by the spleen colony or the 125IUdR-59Fe uptake methods. Growth of DBA/2J (Jackson subline) marrow grafts was poor in irradiated CDF1J hybrids as compared with growth in syngeneic and allogeneic hosts. The DBA/2J transplants proliferated, however, without impairment in irradiated CDF1 hybrids which were the progeny of DBA/2 male parents of other sublines, e.g. DBA/2Ha, DBA/2Cr, and DBA/2Cum. In contrast, tissue-cultured Friend leukemic cells of DBA/2J origin grew deficiently in all CDF1 hybrids tested, regardless of irradiation and of the DBA/2 parent's subline. The growth pattern of transplanted DBA/2J cells was a manifestation of hybrid resistance. The results with DBA/2J and other DBA/2 subline grafts suggested that hybrid histocompatibility alleles were expressed to a greater extent in leukemic than in normal marrow cells, for the former were consistently recognized as "nonself" by CDF1 mice, but not the latter cells. The property of deficient growth in irradiated CDF1Ha hybrids was acquired by DBA/2J hemopoietic cells within 6 hr from infection in vivo with Friend leukemia virus, and persisted during the following 8 days. It was ascribed to enhanced expression of hybrid histocompatibility gene(s) (Hh) induced by the virus. Autonomous growth potential of hemopoietic cells, manifested by proliferation in nonirradiated recipients, was first detected 24 hr from infection, and likewise persisted at the later intervals. At the same time, the infected cells grew deficiently also in nonirradiated CDF1Ha mice. The two irreversible cellular changes were regarded as the earliest signals of virus-induced transformation.

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Involvement of GER in Friend leukemia virus assembly in high-pressure frozen cells

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100160509 ◽

1990 ◽

Vol 48 (3) ◽

pp. 590-591

Author(s):

W. Djaczenko ◽

M. Müller ◽

A. Benedetto ◽

G. Carbone

Keyword(s):

High Pressure ◽

Virus Assembly ◽

Leukemia Virus ◽

Leukemia Cells ◽

Serial Sections ◽

Myeloma Cells ◽

Virus Particles ◽

Friend Leukemia ◽

Carbon Coated ◽

Friend Leukemia Virus

A thickening of ER membranes in murine myeloma cells was attributed by de Harven to the assembly of intracisternal virus particles. We observed similar thickening of GER membranes in Friend leukemia cells (FLC) apparently associated with Friend leukemia virus (FLV) assembly. We reinvestigated the problem of GER involvement in FLV assembly using high pressure cryofixed FLC.FLC (745A clone growing in suspension and FF clone growing in monolayer) were immersed in Hexadecene (Fluka, Switzerland) and rapidly frozen in Balzers HPM 010 freezing machine working at 2200 bar. All cells were freeze substituted at -90°C in 2% OsO4 in absolute acetone. Serial sections cut to avoid misinterpretations due to the geometry of sections, were collected on carbon coated 100 mesh grids.

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Helper Activity for the Defective Friend Leukemia Virus in Human Malignant Cell Cultures

Human Tumor Cells in Vitro ◽

10.1007/978-1-4757-1647-4_16 ◽

1975 ◽

pp. 517-549

Author(s):

Audrey Fjelde

Keyword(s):

Cell Cultures ◽

Leukemia Virus ◽

Malignant Cell ◽

Friend Leukemia ◽

Helper Activity ◽

Friend Leukemia Virus

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What can we learn from Fli1-deficient mice, new animal models of systemic sclerosis?

Journal of Scleroderma and Related Disorders ◽

10.1177/2397198318758221 ◽

2018 ◽

Vol 3 (1) ◽

pp. 6-13 ◽

Cited By ~ 1

Author(s):

Yoshihide Asano

Keyword(s):

Systemic Sclerosis ◽

Animal Models ◽

Leukemia Virus ◽

Environmental Influences ◽

Epidemiological Studies ◽

Potential Candidate ◽

Predisposing Factor ◽

Friend Leukemia ◽

Virus Integration ◽

Friend Leukemia Virus

Systemic sclerosis is a complex multifactorial disease characterized by autoimmunity, vasculopathy, and selective organ fibrosis. A series of genetic and epidemiological studies have demonstrated that environmental influences play a central role in the onset of systemic sclerosis, while genetic factors determine the susceptibility to and the severity of this disease. Therefore, the identification of predisposing factors related to environmental influences would provide us with an informative clue to better understand the pathological process of this disease. Based on this concept, the deficiency of transcription factor Friend leukemia virus integration 1, which is epigenetically suppressed in systemic sclerosis, seems to be a potential candidate acting as the predisposing factor of this disease. Indeed, Fli1-mutated mice serve as a set of useful disease models to disclose the complex pathology of systemic sclerosis. This article overviews the recent advancement in systemic sclerosis animal models associated with Friend leukemia virus integration 1 deficiency.

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