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Molecular and Cellular Biology, January 2007, p. 135-146, Vol. 27, No. 1
0270-7306/07/$08.00+0 doi:10.1128/MCB.01283-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Department of Medicine, Division of Cardiology, NRC3, Oregon Health and Sciences University, 3181 Southwest Sam Jackson Park Road, Portland, Oregon 97239
Received 13 July 2006/ Returned for modification 11 August 2006/ Accepted 26 September 2006
The CBP/p300 family of proteins comprises related acetyltransferases that coactivate signal-responsive transcription. Recent evidence suggests that p300/CBP may also interact directly with complexes that mediate different aspects of DNA metabolism such as replication and repair. In this report, we show that loss of dCBP in Drosophila cells and eye discs results in a defect in the cell cycle arrest induced by stalled DNA replication. We show that dCBP and the checkpoint kinase Mei-41 can be found together in a complex and, furthermore, that dCBP has a genetic interaction with mei-41 in the response to stalled DNA replication. These observations suggest a broader role for the p300/CBP acetyltransferases in the modulation of chromatin structure and function during DNA metabolic events as well as for transcription.
Published ahead of print on 16 October 2006.
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