Abstract
The viral and cellular homologs of the mos oncogene have been useful for studying the molecular elements required for cell transformation. These studies provided the first direct comparison of a viral oncogene and its cellular counterpart (8,14) and demonstrated that the cellular mos could be activated by viral sequences that cause cell transformation (14). Subsequently, it was shown that the proviral.transcription control element or long terminal repeat (LTR) and its enhancer was responsible for activation of the mouse c-mos (1,2,10,21). The more difficult task of identifying the mechanism by which the mos oncogene causes expression of the transformed phenotype remains to be solved. One approach to this problem has been to study proto-oncogene expression which can reveal important information about possible function. However, because the mos proto-oncogene is expressed at very low levels (15), it escaped detection for many years (5,6,13), and we, therefore, studied the biological activity of LTRactivated c-mos as a means of identifying important regulatory elements within the normal proto-oncogene locus. We first discovered an element called the upstream mouse sequence (UMS) located approximately 1.5 kilo-bases (kb) upstream from c-mosmu. This sequence prevented c-mos activation by a downstream LTR (14,22). UMS was subsequently shown to have both polyadenylation and transcription termination functions (12,22). We identified several regions in mos proto-oncogene loci from three different species, mouse (c-mosmff), human (c-moshu) and chicken (c-mosch) (12,22;Schmidt, in preparation) which reduce biological transforming activity. The c-mosmu sequence has been most extensively characterized.
This is an abbreviated form of an article which will appear in the Proceedings of the 14th International Cancer Congress, Budapest, Hungary 8/21-27/86.
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References
BLAIR, D.G.; McCLEMENTS, W.L.;.OSKARSSON, M.K.; FISCHINGER, P.J., and VANDE WOUDE, G.F.: Biological activity of cloned Moloney sarcoma virus DNA: Terminally redundant sequences may enhance transformation efficiency. Proc. Natl. Acad. Sci. USA 77: 3504 - 3508 (1980).
BLAIR, D.G.; OSKARSSON, M.; WOOD, T.G.; McCLEMENTS, W.L.; FISCHINGER, P.J., and VANDE WOUDE, G.F.: Activation of the transforming potential of a normal cell sequence: A molecular model for oncogenesis. Science 212: 941 - 943 (1981).
BLAIR, D.G.; WOOD, T.G.; WOODWORTH, A.M.; McGEADY, M.L.; OSKARSSON, M.K.; PROPST, F.; TAINSKY, M.; COOPER, C.S., WATSON, R.; BAROUDY, B.M., and VANDE WOUDE, G.F.: Properties of the mouse and human mos oncogene loci; in VANDE WOUDE, LEVINE, TOPP, and WATSON, Cancer Cells: Oncogenes and Viral Genes, vol. 2, pp. 281-289 ( Cold Spring Harbor, New York 1984 ).
BLAIR, D.G.; OSKARSSON, M.K.; SETH, A.; DUNN, K.J.; DEAN, M.; ZWEIG, M.; TAINSKY, M.A., and VANDE WOUDE, G.F.: Analysis of the transforming potential of the human homolog of mos. Cell 46: 785 - 794 (1986).
GÄTTONI, S.; KIRSCHMEIER, P.; WEINSTEIN, I.B.,; ESCOBEDO, J., and DINA, D.: Cellular Moloney murine sarcoma (c-mos) sequences are hypermethylated and transcriptionally silent in normal and transformed rodent cells. Mol. Cell. Biol. 2: 42 - 51 (1982).
GOYETTE, M.; PETROPOULOS, C.J.; SHANK, P.R., and FAUSTO, N.: Regulated transcription of c-Ki-ras and c-myc during compensatory growth of rat liver. Mol. Cell. Biol. 4: 1493 - 1498 (1984).
HANNINK, M. and DONOGHUE, D.J.: Lysine residue 121 in the proposed ATP-binding site of the v-mos protein is required for transformation. Proc. Natl. Acad. Sci. USA 82; 7894 - 7898 (1985).
JONES, M.; BOSSELMAN, R.A.; VAN DER HOORN, F.A.; BERNS, A.; FAN, H., and VERMA, I.M.: Identification and molecular cloning of Moloney mouse sarcoma virus-specific sequences from uninfected mouse cells. Proc. Natl. Acad. Sci. USA 77: 2651 - 2655 (1980).
KLOETZER, W.S.; MAXWELL, S.A., and ARLINGHAUS, R.B.: p85gag-mos encoded by ts110 Moloney murine sarcoma virus has an associated protein kinase activity. Proc. Nati. Acad. Sci. USA 80: 412 - 416 (1983).
LEVINSON, B.; KHOURY, G.; VANDE WOUDE, G., and GRUSS, P.: Activation of the SV40 genome by the 72 base-pair tandem repeats of Moloney sarcoma virus. Nature (London) 295: 568 - 572 (1982).
MAXWELL, S.A. and ARLINGHAUS, R.B.: Serine kinase activity associated with Moloney murine sarcoma virus-124-encoded p37m0S. Virology 143: 321 - 333 (1985).
McGEADY, M.L.; WOOD, T.G.; MAIZEL, J.V., and VANDE WOUDE, G.F.: Sequence upstream to the mouse c-mos oncogene may function as a transcription termination signal. DNA, in press.
MULLER, R.; SLAMON, D.J.; TREMBLAY, J.M.; CLINE, M.J., and VERMA, I.M.: Differential expression of cellular oncogenes during pre-and postnatal development of the mouse. Nature 299: 640 - 644 (1982).
OSKARSSON, M.; McCLEMENTS, W.L.; BLAIR, D.G.; MAIZEL, J.V., and VANDE WOUDE, G.F.: Properties of a normal mouse cell DNA sequence (sarc) homologous to the src sequence of Moloney murine sarcoma virus. Science 207: 1222 - 1224 (1980).
PROPST, F. and VANDE WOUDE, G.F.: Expression of c-mos proto-oncogene transcripts in mouse tissues. Nature 315: 516 - 518 (1985).
RECHAVI, G.; GIVOL, D., and CANAANI, E.: Activation of a cellular oncogene by DNA rearrangement. Possible involvement of an IS-like element. Nature 300: 607 - 611 (1982).
SETH, A. and VANDE WOUDE, G.F.: Nucleotide sequence and the biochemical activities of the HT1MSV mos gene. J. Virol. 56: 144 - 152 (1985).
VAN BEVEREN, C.; VAN STRAATEN, F.; GALLESHAW, J.A., and VERMA, A.: Nucleotide sequence of the genome of a murine sarcoma virus. Cell 27: 97 - 108 (1981).
VAN DER HOORN, F.A.; MULLER, V., and PIZER, L.: Sequences upstream of c-mos (rat) that block RNA accumulation in mouse cells do not inhibit in vitro transcription. Mol. Cell. Biol. 5: 406 - 409 (1985).
WATSON, R.; OSKARSSON, M., and VANDE WOUDE, G.F.: Human DNA sequence homologous to the transforming gene (mos) of Moloney murine sarcoma virus. Proc. Natl. Acad. Sci. USA 79: 4078 - 4082 (1982).
WOOD, T.G.; McGEADY, M.L.; BLAIR, D.G., and VANDE WOUDE, G.F.: Long terminal repeat enhancement of v-mos transforming activity: Identification of essential regions. J.Virol. 46: 726 - 736 (1983).
WOOD, T.G.; McGEADY, M.L.; BAROUDY, B.M.; BLAIR, D.G., and VANDE WOUDE, G.F.: Mouse c-mos oncogene activation is prevented by upstream sequences. Proc. Natl. Acad. Sci. USA 81: 7817 - 7821 (1984).
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© 1987 Springer-Verlag Berlin Heidelberg
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McGeady, M.L. et al. (1987). Cis Regulatory Control of mos Oncogene Expression. In: Schettler, G. (eds) Molecular Biology of the Arterial Wall. Veröffentlichungen aus der Geomedizinischen Forschungsstelle der Heidelberger Akademie der Wissenschaften, vol 1987/88 / 1987/4. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-83118-8_24
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