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A role of cyclin G in the process of apoptosis

Oncogene volume 18, pages 4606–4615 (1999)Cite this article

Abstract

Cyclin G was previously identified as a target gene of the p53 tumor suppresser protein, and levels of cyclin G are increased after induction of p53 by DNA damage. However, the function of cyclin G has not been established. To determine the effect of increased expression of cyclin G, retroviruses encoding cyclin G were constructed and used to infect three different murine cell lines. Cyclin G protein levels induced by the retroviruses were within the range seen after DNA damage induction of p53. In each case we observed that such over-expression of cyclin G augments the apoptotic process. TNF-α induction of apoptosis is increased by expression of cyclin G in NIH3T3 fibroblasts which express p53, as well as in 10.1 fibroblasts which contain no p53 allele. Additionally, we observed that while cyclin G expression is markedly reduced upon aggregate formation in embryonic carcinoma P19 cells, retrovirus-mediated over-expression of cyclin G enhances apoptotic cell death in aggregated P19 cells, and increases the extent of apoptosis caused by retinoic acid or serum starvation of these cells. These data demonstrate that cyclin G plays a facilitating role in modulating apoptosis induced by different stimuli. Moreover, we have discovered that cyclin G expression is rapidly induced in P19 cells after exposure to Bone Morphogenic Protein-4 (BMP-4), suggesting that cyclin G may mediate apoptotic signals generated by BMP-4.

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Acknowledgements

We thank Paul B Robbins for the retrovirus vector, Jill Bargonetti for 10.1 cells, and Ella Freulich for technical support. BMP-4 was a generous gift from Genetics Institute. These studies were supported by NIH grant CA58316.

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  1. Department of Biological Sciences, Columbia University, New York, NY 10027, USA

    Koji Okamoto & Carol Prives

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Okamoto, K., Prives, C. A role of cyclin G in the process of apoptosis. Oncogene 18, 4606–4615 (1999). https://doi.org/10.1038/sj.onc.1202821

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