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Mol. Cell. Biol. doi:10.1128/MCB.01283-06
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Drosophila dCBP is involved in establishing the DNA replication checkpoint

Department of Medicine, Division of Cardiology, mail code NRC3, Oregon Health & Sciences University, 3181 S. W. Sam Jackson Park Road, Portland, Oregon 97239

^* To whom correspondence should be addressed. Email: smoliks{at}ohsu.edu,

	Abstract

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.

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