A selective temperature-sensitive defect in viral RNA expression in cells infected with a ts transformation mutant of murine sarcoma virus

Horn, Jacqueline Peltier; Wood, Theodore; Murphy, Edwin C.; Blair, Donald G.; Arlinghaus, Ralph B.

doi:10.1016/0092-8674(81)90229-4

Cited by 48 publications

(60 citation statements)

References 21 publications

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“…The Immune Complex Kinase Activity Correlates with the Presence of P859'9-' Previous studies have established that P855ag5'-is not detected at 390C, the temperature that is nonpermissive for fibroblast transformation (7,8). Therefore, if the Mr 85,000 protein phosphorylated in the immune complex kinase reaction is indeed P85gag-ms, it should be absent from immune complex kinase reaction products of tsllO-infected 6m2 cells maintained at 390C.…”

Section: Resultsmentioning

confidence: 99%

“…The expression of P85"ag"' in these cells is temperature dependent because only P589ag is detected in cells maintained at 39°C. Such cells grown at 39°C lose characteristics usually associated with the transformed state (7)(8)(9).…”

mentioning

confidence: 99%

“…The v-mos gene has an open reading frame allowing for the translation of a Mr42,000-44,000 protein which is expressed in trace amounts in cells transformed by the 124 strain of Mo-MuSV (5). Work in our laboratory has characterized a variant of Mo-MuSV-124, known as tsllO MuSV, that codes for a gag-mos polyprotein of Mr 85,000 termed P8599-"°as well as for a P58gag (6)(7)(8). A nonproducer cell clone transformed by tsllO MuSV expresses easily detectable levels of both proteins at 33°C.…”

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confidence: 99%

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P85 ^gag-mos encoded by ts110 Moloney murine sarcoma virus has an associated protein kinase activity

Kloetzer

Maxwell

Arlinghaus

1983

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

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A protein identified as P859'9-°was shown to be phosphorylated when immunoprecipitates from tsllO Moloney murine sarcoma virus transformed nonproducer cells (clone 6m2) were incubated with [y-32P]ATP. The in vitro-labeled 85,000-dalton phosphoprotein comigrated on NaDodSO4/polyacrylamide gels with authentic phosphorylated P859'9-°. Immunoprecipitates obtained with antisera prepared against Rauscher murine leukemia virus core protein p30 were active in the immune complex kinase assay but anti-murine leukemia virus plO precipitates were not. Previous studies have shown that anti-p30 but not antiplO antisera recognize P859'9-°. The 6m2 clone has been shown to express P85gag-"w8 at 330C but not at 39TC. Anti-p30 immune complexes from 6m2 cells maintained at 390C failed to phosphorylate the 85,000-dalton protein. Furthermore, the in vitro phosphorylated 85,000-dalton protein gave the same pattern of V8 protease-generated cleavage products as in vivo 32P-labeled P85gag-'.8, We conclude from these results that P85gag`m06 is phosphorylated in anti-p30 immune complex kinase reactions. Phosphoamino acid analyses indicated that the in vitro phosphorylated P85gag-tno contained phosphoserine and phosphothreonine. Our findings indicate that incubation of anti-p30 immunoprecipitates at 39°C drastically reduced, in a specific way, the kinase activity associated with P85gag-1l8. This result and other data suggest that the kinase is virus-encoded. Because P85gag-"1w8, but not Pr65gag, is phosphorylated in anti-p30 immunoprecipitates from MuLVMuSV tsllO producer cells, the kinase enzyme is associated with P85gag-' and not gag gene products. A second major polypeptide of the size of P58gag was also phosphorylated in anti-p30 immunoprecipitates from cells maintained at 33°C but not at 39°C. Since 6m2 cells at 39°C contain P58wag, this is also consistent with the kinase activity being associated with P85gag-11W.

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Section: Resultsmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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P85 ^gag-mos encoded by ts110 Moloney murine sarcoma virus has an associated protein kinase activity

Kloetzer

Maxwell

Arlinghaus

1983

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

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“…The cells were incubated at 37°C under a humidified atmosphere containing 7.5% CO2. L6E9-E cells were obtained by recloning the L6E9 cells infected with Moloney murine sarcoma virus tsllO (27) in 96-well plates. The cells were maintained in DME medium supplemented with 10% FCS at 33°C under 7.5% CO2.…”

Section: Methodsmentioning

confidence: 99%

Transcriptional and posttranscriptional control of c-myc during myogenesis: its mRNA remains inducible in differentiated cells and does not suppress the differentiated phenotype.

Endo¹,

Nadal-Ginard²

1986

Mol. Cell. Biol.

160

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It is widely accepted that the cellular oncogene c-myc plays an important role in the control of cell proliferation and that its expression diminishes in differentiated cells. We examined whether there is a correlation between c-myc expression and cell proliferation or differentiation by using a subclone of a rat skeletal muscle cell line L6E9. Myoblasts irreversibly withdraw from the cell cycle, fuse to form multinucleated myotubes, and express muscle-specific genes (terminal differentiation). Muscle-specific genes can also be expressed in the absence of fusion (biochemical differentiation). Such mononucleated but biochemically differentiated cells can be stimulated to reenter the cell cycle. c-myc was induced by insulin, insulin-like growth factor, or serum factors in GO-arrested cells, whereas induction by protein synthesis inhibitors or superinduction by protein synthesis inhibitors in combination with serum factors occurred in all physiological states tested. We found that c-myc expression was reduced in biochemically and terminally differentiated cells as well as in quiescent undifferentiated cells but that it remained inducible by growth factors in all three physiological states. Results of nuclear runoff transcription assays suggested that the induction of c-myc mRNA by growth factors and its deinduction in these physiological states were regulated mainly at the transcriptional level. In contrast, induction and superinduction of c-myc mRNA by protein synthesis inhibitors alone and in combination with growth factors, respectively, were regulated posttranscriptionally mainly by stabilization of c-myc mRNA. Moreover, c-myc and muscle-specific genes could be simultaneously transcribed in both biochemically and terminally differentiated cells. These results indicate that irreversible repression of c-myc is not required for terminal myogenic differentiation and that its expression is insufficient by itself to suppress the differentiated phenotype.

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“…The mos gene is a retrovirus oncogene, and its product is located at the cytoplasm with threonine-serine kinase activity (14). We compared the effects of transfection of v-mos on transformation of BALB/3T3 and MO-5.…”

Section: Resultsmentioning

confidence: 99%

Transformation by viral and cellular oncogenes of a mouse BALB/3T3 cell mutant resistant to transformation by chemical carcinogens.

Ono¹,

Yakushinji²,

Segawa³

et al. 1988

Mol. Cell. Biol.

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A selective temperature-sensitive defect in viral RNA expression in cells infected with a ts transformation mutant of murine sarcoma virus

Cited by 48 publications

References 21 publications

P85 ^gag-mos encoded by ts110 Moloney murine sarcoma virus has an associated protein kinase activity

P85 ^gag-mos encoded by ts110 Moloney murine sarcoma virus has an associated protein kinase activity

Transcriptional and posttranscriptional control of c-myc during myogenesis: its mRNA remains inducible in differentiated cells and does not suppress the differentiated phenotype.

Transformation by viral and cellular oncogenes of a mouse BALB/3T3 cell mutant resistant to transformation by chemical carcinogens.

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A selective temperature-sensitive defect in viral RNA expression in cells infected with a ts transformation mutant of murine sarcoma virus

Cited by 48 publications

References 21 publications

P85 gag-mos encoded by ts110 Moloney murine sarcoma virus has an associated protein kinase activity

P85 gag-mos encoded by ts110 Moloney murine sarcoma virus has an associated protein kinase activity

Transcriptional and posttranscriptional control of c-myc during myogenesis: its mRNA remains inducible in differentiated cells and does not suppress the differentiated phenotype.

Transformation by viral and cellular oncogenes of a mouse BALB/3T3 cell mutant resistant to transformation by chemical carcinogens.

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P85 ^gag-mos encoded by ts110 Moloney murine sarcoma virus has an associated protein kinase activity

P85 ^gag-mos encoded by ts110 Moloney murine sarcoma virus has an associated protein kinase activity