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Biomedical subjects

M Hatanaka

Publications and source records attributed to M Hatanaka.

At least 379 records · Page 21Linked to original sources
PubMed1974

Sarcoma-virus-related RNA sequences in normal rat cells.

A rat type C virus spontaneously activated from the NRK (normal rat kidney) cell line was found to have two major size classes of viral RNA subunits sedimenting at 35 and 30 S. Virus-producing cells contained both RNA species, while normal "virus-free" rat cells contained primarily virus-specific 30S RNA species. A DNA transcript, specific for Kirsten sarcoma virus, prepared from virus activated in nonproducer BALB/c cells originally transformed by Kirsten sarcoma virus and rendered specific for the virus by absorption of sequences related to mouse helper virus hybridized only with the 30S RNA species of virus-producing rat cells and normal rat cells. These findings are consistent with the hypothesis that sarcoma-specific nucleic acid sequences in kirsten sarcoma virus emerged through a process that incorporated some portions of 30S RNA species from rat cells (either normal or virus-producing) into the Kirsten leukemia virus during passage in vivo of that virus. The virus designated M-MSV(RaLV), which originally derived from tumor induced by Moloney sarcoma virus (M-MSV) in rats, contained 35S RNA species of rat type C viruses and 30S RNA species specific for both rat and mouse viruses. It appears striking that for these two animal species, sarcoma-virus-specific information resides on a 30S subunit.

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PubMed1974

Specificity of the DNA product of RNA-dependent DNA polymerase in type C viruses: 3. Analysis of viruses derived from Syrian hamsters.

DNA transcripts were prepared from three related viruses of hamster and analyzed by interviral hybridization and by reaction with cellular DNA. A virus (G-HaLV), isolated from a dimethylbenzanthraceneinduced tumor cell in Graffi hamsters, contained nucleic acid sequences highly specific for hamster cell DNA and did not react with mouse cell DNA nor did its transcript show homology (<5%) with mouse or rat viral RNAs. The hamster-specific sarcoma virus, B-34, isolated by Bassin and coworkers from tumors induced by the Harvey strain of murine sarcoma virus, contained mouse-, hamster-, and possibly rat-specific sequences. B-34 transcripts were predominantly mouse-specific. GLOH(-), a lymphomagenic virus derived by dilution beyond the transforming endpoint of a hamster-specific sarcoma virus obtained from tumors induced by the Gross pseudotype of murine sarcoma virus, also contained hamster- and mouse-specific sequences. Only a portion of its hamster sequence (about 50%) was shared with B-34 and G-HaLV viruses. As expected, transcripts of GLOH(-) virus were reactive with mouse and hamster cellular DNA.

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PubMed1974

Sarcoma and helper-specific RNA tumor virus subunits in transformed nonproducer mouse cells activated to produce virus by treatment with bromodeoxyuridine.

A tumor line (58-2T) was established from a slowly growing tumor in a BALB/c mouse inoculated with M58-2 cells. The latter clonal cell line was isolated after bromodeoxyuridine treatment as a flat variant from nonproducer BALB/3T3 cells transformed by the Kirsten sarcoma virus. The 58-2T cells produced type C virus with two discrete virus-specific RNA species. One of the species, which was probably an endogenous virus RNA subunit, had a sedimentation coefficient of 35S as the largest major subunit, and had sequences similar to Rauscher leukemia virus RNA based on nucleic acid hybridization. The other RNA species had 30S as the largest major subunit and corresponded to Kirsten sarcoma virus-specific RNA. These two RNA species formed heterogeneous, 60 to 70S, high-molecular-weight RNA in virions.DNA transcripts (58-2T DNA) from the activated virus contained base sequences complementary to Rauscher leukemia virus and Kirsten sarcoma virus. The Kirsten sarcoma virus-specific DNA sequences (58-2TS) were purified from 58-2T DNA by eliminating RLV-specific sequences.

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PubMed1973

Mutants of nonproducer cell lines transformed by murine sarcoma viruses. I. Induction, isolation, particle production, and tumorigenicity.

A variety of cell mutants were obtained by a single 5'-bromodeoxyuridine (BrdU) treatment of an nonproducer (NP) cell line transformed by the Kirsten strain of murine sarcoma virus (Ki-MSV). Isolation procedures of these cell See PDF for Structure mutants are described. The cell mutants obtained were classified by tumorigenic potential and shedding of Type C virus particles. The cell mutants were classified into four groups: (A) tumorigenic, without particles; (B) tumorigenic, with Type C particles; (C) nontumorigenic, without particles; and (D) nontumorigenic, with Type C particles. The tumorigenic cell lines showed variability in morphology with both flat and typical transformed appearing cell lines showing equal transplantability.

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PubMed1973

Mutants of nonproducer cell lines transformed by murine sarcoma virus. II. Relationship of tumorigenicity to presence of viral markers and rescuable sarcoma genome.

Tumorigenic and nontumorigenic mutants induced by a single 5'-bromodeoxyuridine (BrdU) treatment of a nonproducer (NP) tumorigenic cell line were isolated and characterized. Among the cloned derivatives were examples of virus-free and sarcoma virus-producing cell lines. Oncogenicity did not correlate with production of virus or ease of rescue of the sarcoma genome. All lines, including nononcogenic derivatives, retained the sarcoma genome. Phenotypic reversion of some cell mutants was observed after in vivo inoculation or long term in vitro cultivation. The M-50T cell line, obtained from a tumor induced by M-50 cells, had a sarcoma genome rescuable by direct superinfection; this was only achieved with parental M-50 cells by a cell fusion rescue technique. The M-43-2T cell, obtained from a single small static tumor induced by otherwise nononcogenic M-43-2 cells, shed sarcoma virus and became tumorigenic. M-58-4-48 became tumorigenic after passage 48 of the M-58-4 line, which was originally nontumorigenic. These observations of phenotypic reversion demonstrate that the presence of the sarcoma gene in cells is an essential but not sufficient condition of tumorigenesis.

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PubMed1973

Specificity of the DNA product of RNA-dependent DNA polymerase in type C viruses. II. Quantitative analysis.

A number of mammalian Type C viruses were analyzed for relatedness by the technique of DNA.RNA hybridization. Viral DNAs were prepared in single-stranded form from complexes with 70S viral RNA formed during endogenous polymerase reactions. Extent of hybridization was assayed with the single-strand nuclease (S-1) from Aspergillus oryzae. Results obtained indicated a high degree of viral specificity, with significant cross-reactions being observed only with viruses obtained from within a species, as in the case of mouse and cat viruses, or in the special case of woolly monkey-gibbon comparisons. Comparisons of RD-114 virus, recently determined to be of feline origin, and conventional feline Type C viruses (FeLV), revealed minimal relatedness, especially when feline virus was grown on human cells, thus indicating the possibility of coexistence of greatly disparate Type C viruses within one species. A rat-specific virus, recovered from tumors induced by murine sarcoma virus, was found to contain genetic material common to both the original mouse virus and viruses indigenous to the rat, even though only rat-specific proteins have been detected during infection by this virus.

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PubMed1973

Sugar effects on murine sarcoma virus transformation.

Transformation of NIH Swiss mouse fibroblasts by a murine sarcoma virus was influenced by the type of carbohydrate in the culture medium. Exposure to D-mannose and 2-deoxy-D-glucose caused a reduction in the number of transformed colonies in vitro and tumor formation in vivo. This is a new type of interference in the transformation process, manifested also by the absence of the pronounced enhancement of hexose entry into transformed cells, characteristic of a sarcoma virus infection. The uptake of D-glucose, D-mannose, and D-galactose, was repressed by normal mouse cells grown in the presence of D-mannose and D-glucose in the medium, while uptake of the same sugars was derepressed in cells grown in media containing D-xylose, L-xylose, or L-arabinose. D-Galactose had an intermediate effect on hexose uptake and permitted derepression. In every case, enhancement of the primary transport by sarcoma virus transformation was consistently beyond that observed at any time in the derepressed control cells, demonstrating the occurrence of another mechanism of enhancement of hexose uptake after sarcoma virus infection.

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