Moloney Leukaemia Virus as a Helper in retrieving Friend Virus from a Non-infectious Reticulum Cell Sarcoma

Fieldsteel, A H; Kurahara, Carole; Dawson, Peter J.

doi:10.1038/2231274a0

Cited by 32 publications

(8 citation statements)

References 5 publications

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“…No specific binding of125I-Epo was observed for any of the following cell lines; human erythroleukemia HEL and K-562 cells, mouse myelomonocytic leukemia WEHI-3 cells, human promyelocytic letikemia HL-60 cells, mouse IL-3 dependent P cell-like IC-2 cells (16) and mouse reticulum sarcoma FVTCT cells (17). Even when the concentration of 125I-Epo was increased to 5 nM, no specific binding could be detected on these cells.…”

Section: Resultsmentioning

confidence: 95%

Specific binding of erythropoietin to its receptor on responsive mouse erythroleukemia cells.

Todokoro¹,

Kanazawa²,

Arima³

et al. 1987

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

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Erythropoietin (Epo) is a glycoprotein factor that specifically regulates the proliferation and differentiation of erythroid progenitor cells. Here we describe the isolation of Epo-responsive mouse erythroleukemia cell line SKT6, the characterization of the specific binding of biologically active '25I-labeled human Epo ('25I-Epo) to its membrane receptor, and, finally, report information concerning the molecular structure of the receptor. About 75% of erythroid colonyforming precursor cell-like colonies derived from SKT6 cells were hemoglobin-positive after 3-to 4-day exposure to Epo in methylcellulose culture. Radioiodinated Epo bound specifically to SKT6 cells, and Scatchard analysis of the data showed a high affinity for 125I-Epo (Kd = 0.15 nM) but displayed only a small number of specific receptors (=470 per cell). Membrane components that specifically interact with 125I-Epo were identified by covalent crosslinking with disuccinimidyl suberate, and three receptor species with apparent Mr 63,000, 94,000, and 119,000 were found in membrane from SKT6 cells, suggesting the complex structure of the receptor molecules. Specific bindings were also detected in all of the Epo-unresponsive Friend erythroleukemia cells examined, and crosslinking study revealed the presence of only the 63,000 species as a binding site.

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Section: Resultsmentioning

confidence: 95%

Specific binding of erythropoietin to its receptor on responsive mouse erythroleukemia cells.

Todokoro¹,

Kanazawa²,

Arima³

et al. 1987

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

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“…In order to study the action of BrdUrd on virus replication and its role in the induction of endogenous virus we have used Friend virus (FV) infected and transformed DBA-2 mouse spleen cells in culture. The FV complex consists of two components, the lymphatic leukemia helper virus (LLV-F) and the replication-defective erythroid cell-transforming spleen focus-forming virus (SFFV-F) (5,6). The RNA of the two virus types is presumably different in size and structure (7).…”

mentioning

confidence: 99%

Induction of Endogenous Virus and of Thymidine Kinase by Bromodeoxyuridine in Cell Cultures Transformed by Friend Virus

Ostertag

Roesler

Krieg

et al. 1974

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

105

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Thymidine kinase positive (TK+) N type cell lines that had been transformed by spleen focus-forming virus were established by transformation with NB tropic Friend virus complex. Thymidine kinase deficient (TK-) cell clones were isolated. Some of these cell clones release 1000-to 100,000-fold reduced amounts of Friend virus complex as compared to the TK+ parental cell clone. TK-clones were grown in medium without BrdUrd. Some of these TK-clones can be induced to release endogenous helper virus and transforming spleen focus-forming virus on reexposure to 10-10-4 M BrdUrd. BrdUrd inhibits the replication of C-type tumor viruses (1), whereas in some instances BrdUrd or IdUrd can induce endogenous C-type virus (2-4). In order to study the action of BrdUrd on virus replication and its role in the induction of endogenous virus we have used Friend virus (FV) infected and transformed DBA-2 mouse spleen cells in culture. The FV complex consists of two components, the lymphatic leukemia helper virus (LLV-F) and the replication-defective erythroid cell-transforming spleen focus-forming virus (SFFV-F) (5, 6). The RNA of the two virus types is presumably different in size and structure (7). We have established various cell lines transformed by the SFFV-F (8, 9) which, after another thymidine analogue, can be phosphorylated to azidothymidine triphosphate. However, the presence of an No group at the 3' terminal of the deoxysugar interferes with esterification, so presumably azidothymidine can only be added terminally to the growing DNA strand. Both azidothymidine as well as BrdUrd can be used to decrease the virus titer of BrdUrd-sensitive erythroleukemic cells. We have isolated several BrdUrd-resistant clones by treatment of sensitive cells with high doses of BrdUrd (11) and have shown that some of these clones have either decreased or barely detectable thymidine kinase (ATP: thymidine 5'-phosphotransferase, EC 2.7.1.75) activity (11). Furthermore, they have a 108-to 104-fold decreased virus titer. The decrease in C-type virus release can also be shown by electron microscopy.A temporary thymidine kinase activation is observed if BrdUrd is added to some virus negative lines. The same cells release large numbers of endogenous C-type and spleen focusforming virus on exposure to BrdUrd but not to azidothymidine. The RNA tumor virus which is induced by BrdUrd has mainly N-type host range properties unlike the original NB type FV complex which has been used for the transformation of our erythroid cell lines. Thymidine kinase induction and virus induction are always correlated. We have independent evidence (Ostertag, Crozier, and Swetly, unpublished)

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“…The lymphoid leukemia virus can be obtained free of the spleen focus-forming virus, but the reverse seems not possible, indicating some dependence of the spleen focus-forming virus on the lymphoid leukemia agent for replication (Dawson et ai., 1968;Rowson and Parr, 1970;Steeves et al, 1971). A nonproducing cell line from a Friend virus-induced reticulum cell sarcoma has been isolated, and Friend virus can be rescued from this line by superinfection with murine lymphoid or myeloid leukemia virus in tissue culture or in the animal (Fieldsteel et al, 1969(Fieldsteel et al, ,1971. The spleen focus-forming virus produced under these conditions and probably all spleen focus-forming components of the Friend murine leukemia virus are pseudotypes.…”

Section: Replication-defective Murine Leukemia Viruses Are Alsomentioning

confidence: 97%

Genetics of RNA Tumor Viruses

Vogt

1977

Regulation and Genetics

105

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Moloney Leukaemia Virus as a Helper in retrieving Friend Virus from a Non-infectious Reticulum Cell Sarcoma

Cited by 32 publications

References 5 publications

Specific binding of erythropoietin to its receptor on responsive mouse erythroleukemia cells.

Specific binding of erythropoietin to its receptor on responsive mouse erythroleukemia cells.

Induction of Endogenous Virus and of Thymidine Kinase by Bromodeoxyuridine in Cell Cultures Transformed by Friend Virus

Genetics of RNA Tumor Viruses

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