Distinct roles of the co-activators p300 and CBP in retinoic-acid-induced F9-cell differentiation

Hiroaki Kawasaki, Richard Eckner, Tso-Pang Yao, Kazunari Taira, Robert Chiu, David M. Livingston and Kazunari K. Yokoyama ()
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Hiroaki Kawasaki: Tsukuba Life Science Center, The Institute of Physical and Chemical Research (RIKEN)
Richard Eckner: Institute for Molecular Biology, University of Zürich
Tso-Pang Yao: Dana-Farber Cancer Institute and Harvard Medical School
Kazunari Taira: Institute of Applied Biochemistry, University of Tsukuba
Robert Chiu: UCLA School of Medicine and Jonsson Comprehensive Cancer Centre
David M. Livingston: Dana-Farber Cancer Institute and Harvard Medical School
Kazunari K. Yokoyama: Tsukuba Life Science Center, The Institute of Physical and Chemical Research (RIKEN)

Nature, 1998, vol. 393, issue 6682, 284-289

Abstract: Abstract The related proteins p300 and CBP (cAMP-response-element-binding protein (CREB)-binding protein)) are transcriptional co-activators that act with other factors to regulate gene expression1,2,3,4,5 and play roles in many cell-differentiation and signal transduction pathways6,7,8,9,10. Both proteins have intrinsic histone-acetyltransferase activity11,12 and may act directly on chromatin, of which histone is a component, to facilitate transcription. They are also involved in growth control pathways, as shown by their interaction with the tumour suppressor p53 (13–15) and the viral oncogenes E1A (refs 1, 2, 16) and SV40 T antigen5. Here we report functional differences of p300 and CBP in vivo. We examined their roles during retinoic-acid-induced differentiation, cell-cycle exit and programmed cell death (apoptosis) of embryonal carcinoma F9 cells17,18,19,20, using hammerhead ribozymes capable of cleaving either p300 or CBP messenger RNAs. F9 cells expressing a p300-specific ribozyme became resistant to retinoic-acid-induced differentiation, whereas cells expressing a CBP-specific ribozyme were unaffected. Similarly, retinoic-acid-induced transcriptional upregulation of the cell-cycle inhibitor p21Cip1 required normal levels of p300, but not CBP, whereas the reverse was true for p27Kip1. In contrast, both ribozymes blocked retinoic-acid-induced apoptosis, indicating that both co-activators are required for this process. Thus, despite their similarities, p300 and CBP have distinct functions during retinoic-acid-induced differentiation of F9 cells.

Date: 1998
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DOI: 10.1038/30538

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