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EMBO reports 7, 12, 1266–1272 (2006)
doi:10.1038/sj.embor.7400851
AOP Published online: 10 November 2006
Molecular dissection of the APC/C inhibitor Rca1 shows a novel F-box-dependent function
Norman Zielke1, Silvia Querings1, Ruth Grosskortenhaus1†, Tânia Reis2‡ & Frank Sprenger1
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1 Institute for Genetics, University of Cologne, Zülpicherstrasse 47, 50674 Köln, Germany
2 Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N, PO Box 19024, Seattle, Washington 98109, USA
To whom correspondence should be addressed
Frank Sprenger Tel: +49 221 470 5259; Fax: +49 221 470 5264; E-mail: sprenger@uni-koeln.de
† Present address: Biotechnologisches Zentrum, Technische Universität Dresden, Tatzberg 47-51, 01307 Dresden, Germany
‡ Present address: Department of Molecular and Cell Biology, UC Berkeley, 142 Life Science Addition, Berkeley, California 94720-3200, USA
Received 17 May 2006; Accepted 27 September 2006; Published online 10 November 2006.
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Abstract
Rca1 (regulator of Cyclin A)/Emi (early mitotic inhibitor) proteins are essential inhibitors of the anaphase-promoting complex/cyclosome (APC/C). In Drosophila, Rca1 is required during G2 to prevent premature cyclin degradation by the Fizzy-related (Fzr)-dependent APC/C activity. Here, we present a structure and function analysis of Rca1 showing that a carboxy-terminal fragment is sufficient for APC/C inhibition. Rca1/Emi proteins contain a conserved F-box and interact with components of the Skp–Cullin–F-box (SCF) complex. So far, no function has been ascribed to this domain. We find that the F-box of Rca1 is dispensable for APC/C–Fzr inhibition during G2. Nevertheless, we show that Rca1 has an additional function at the G1–S transition, which requires the F-box. Overexpression of Rca1 accelerates the G1–S transition in an F-box-dependent manner. Conversely, S-phase entry is delayed in cells in which endogenous Rca1 is replaced by a transgene lacking the F-box. We propose that Rca1 acts as an F-box protein in an as yet uncharacterized SCF complex, which promotes S-phase entry.
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