Abstract
Before quiescent cells can respond to mitogens and progress through the G1 phase of cell growth, new messenger RNA synthesis is required1. The G1 phase seems to be a critical point of control in the cell cycle, where normal cells deprived of growth factors halt cycling while transformed cells do not, suggesting that regulatory genes, uncontrolled in the neoplastic phenotype, are expressed during the G0 to G1 transition. Some of these may code for nuclear proteins that participate in the transactivation of genes required for the progression through G1. The observed changes in expression of the proto-oncogenes c-fos and c-myc, following stimulation of fibroblasts with growth factors2–7, support this notion as recent evidence suggests that c-FOS and c-MYC proteins can function as transactivating factors8–12. Moreover, the rapid induction of several genes in fibroblasts coding for putative transacting factors during the G0 to G1 transition has been recently reported13–16. Here we present the nucleotide sequence of a mouse cDNA clone coding for a 334 residue protein which shows 80% similarity with v-JUN17 and more than 98% similarity with the human c-JUN sequence18,19. We have demonstrated that in quiescent fibroblasts c-jun transcription is rapidly induced during the G0 to G1 transition.
This is a preview of subscription content, access via your institution
Access options
Subscribe to this journal
Receive 51 print issues and online access
$199.00 per year
only $3.90 per issue
Buy this article
- Purchase on Springer Link
- Instant access to full article PDF
Prices may be subject to local taxes which are calculated during checkout
Similar content being viewed by others
References
Baserga, R. in Biology of Cell Reproduction (ed. Baserga, R.) 107–112 (Harvard University Press, Cambridge, 1985).
Kelly, K., Cochran, B. H., Stiles, C. D. & Leder, P. Cell 35, 603–610 (1983).
Cochran, B. H., Zullo, J., Verma, I. M. & Stiles, C. D. Science 226, 1080–1082 (1983).
Greenberg, M. E. & Ziff, E. B. Nature 311, 433–438 (1984).
Kriujer, W., Cooper, J. A., Hunter, T. & Verma, I. M. Nature 312, 711–716 (1984).
Müller, R., Bravo, R., Burckhardt, J. & Curran, T. Nature 312, 716–720 (1984).
Bravo, R., Macdonald-Bravo, H., Müller, R., Hübsch, D. & Almendral, J. M. Expl. Cell Res. 170, 103–115 (1987).
Kaddurah-Daouk, R., Greene, J. M., Baldwin, A. S. & Kingston, R. E. Genes Dev. 1, 347–357 (1987).
Distel, R. J., Ro, H. S., Rosen, B. S., Groves, D. L. & Spiegelmann, B. M. Cell 49, 835–844 (1987).
Kingston, R. E., Baldwin, A. S. & Sharp, P. A. Nature 212, 280–282 (1984).
Rauscher, F. S., Sambrucetti, L. D., Curran, T., Distel, R. J. & Spiegelman, B. M. Cell 52, 471–480 (1988).
Lech, K., Anderson, K. & Brent, R. Cell 52, 179 (1988).
Ryder, K., Lau, L. F. & Nathans, D. Proc. natn. Acad. Sci. U.S.A. 85, 1487–1491 (1988).
Chavrier, P. et al. EMBO J. 7, 29–35 (1988).
Lemaire, P., Revelant, O., Bravo, R. & Charnay, P. Proc. natn. Acad. Sci. U.S.A. 85, 4691–4695 (1988).
Sukhatme, V. P. et al. Cell 53, 37–43 (1988).
Maki, Y., Bos, C., Davis, C., Starbuck, M. & Vogt, P. Proc. natn. Acad. Sci. U.S.A. 84, 2848–2852 (1987).
Bohmann, F. et al. Science 238, 1386–1392 (1987).
Angel, P. et al. Nature 332, 166–171 (1988).
Almendral, J. M. et al. Molec. cell. Biol 99, (in the press).
Birnstiel, M. L., Burslinger, M. & Strub, K. Cell 41, 349–351 (1985).
Shaw, G. & Kamen, R. Cell 46, 659–667 (1986).
Piette, J., Hirai, S. I. & Yaniv, M. Proc. natn. Acad. Sci. U.S.A. (in the press).
Nishikura, K. & Murray, J. M. Molec. cell. Biol. 77, 639–649 (1987).
Heikkla, R. et al. Nature 328, 445–449 (1987).
Messing, J. Meth. Enzym. 101, 20–78 (1983).
Sanger, F., Nicklen, S. & Coulson, A. R. Proc. natn. Acad. Sci. U.S.A. 74, 5463–5467 (1977).
Chirgwin, J. M., Przylyl, A. E., Macdonald, R. J. & Rutter, W. J. Biochemistry 18, 5294–5299 (1979).
Maniatis, T., Fritsch, E. F. & Sambrook, J. Molecular Cloning (Cold Spring Harbor Laboratory, New York, 1982).
Thomas, P. S. Proc. natn. Acad. Sci. U.S.A. 77, 5201–5205 (1980).
Langridge, J., Langridge, P. & Berquist, P. L. Analyt. Biochem. 103, 264–271 (1980).
Rigby, P. W. J., Dieckmann, M., Rhodes, C. & Berg, P. Proc. natn. Acad. Sci. U.S.A. 74, 5463–5467 (1977).
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Ryseck, RP., Hirai, S., Yaniv, M. et al. Transcriptional activation of c-jun during the G0/G1 transition in mouse fibroblasts. Nature 334, 535–537 (1988). https://doi.org/10.1038/334535a0
Received:
Accepted:
Published:
Issue Date:
DOI: https://doi.org/10.1038/334535a0
This article is cited by
-
The E3 ubiquitin ligase Trim7 mediates c-Jun/AP-1 activation by Ras signalling
Nature Communications (2015)
-
N-(2-hydroxy phenyl) acetamide produces profound inhibition of c-Fos protein and mRNA expression in the brain of adjuvant-induced arthritic rats
Molecular and Cellular Biochemistry (2014)
-
Emerging roles of ATF2 and the dynamic AP1 network in cancer
Nature Reviews Cancer (2010)
-
Oxalate exposure provokes HSP 70 response in LLC-PK1 cells, a line of renal epithelial cells: protective role of HSP 70 against oxalate toxicity
Urological Research (2008)
-
Estrogen-induced proliferation of normal endometrial glandular cells is initiated by transcriptional activation of cyclin D1 via binding of c-Jun to an AP-1 sequence
Oncogene (2004)
Comments
By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate.
