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Published on May 20, 2009; 10.1104/pp.109.140269

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Received April 22, 2009
Accepted May 15, 2009

CDKB1;1 forms a functional complex with CYCA2;3 to suppress endocycle onset

Veronique Boudolf , Tim Lammens , Joanna Boruc , Jelle Van Leene , Hilde Van Den Daele , Sara Maes , Gert Van Isterdael , Eugenia Russinova , Eva Kondorosi , Erwin Witters , Geert De Jaeger , Dirk Inze , and Lieven De Veylder *

Department of Plant Systems Biology, Flanders Institute for Biotechnology (VIB), 9052 Ghent, Belgium; Department of Plant Biotechnology and Genetics, Ghent University, 9052 Ghent, Belgium; Institut des Sciences du Vegetal, Centre National de la Recherche Scientifique, Unite Propre de Recherche 2355, 91198 Gif-sur-Yvette, France; Institute for Plant Genomics, Human Biotechnology and Bioenergy, Bay Zoltan Foundation for Applied Research, 6726 Szeged, Hungary; Center for Proteome Analysis and Mass Spectrometry, University of Antwerp, 2020 Antwerpen, Belgium; Flemish Institute for Technological Research (VITO), 2400 Mol, Belgium

* Corresponding author; email: lieven.deveylder{at}psb.vib-ugent.be.

The mitosis-to-endocycle transition requires the controlled inactivation of M-phase-associated cyclin-dependent kinase (CDK) activity. Previously, the B-type CDKB1;1 has been identified as an important negative regulator of endocycle onset. Here, we demonstrate that CDKB1;1 co-purifies and associates with the A2-type cyclin CYCA2;3. Co-expression of CYCA2;3 with CDKB1;1 triggered ectopic cell divisions and inhibited endoreduplication. Moreover, the enhanced endoreduplication phenotype observed after overexpression of a dominant-negative allele of CDKB1;1 could be partially complemented by CYCA2;3 co-overexpression, illustrating that both subunits unite in vivo to form a functional complex. CYCA2;3 protein stability was found to be controlled by CCS52A1, an activator of the anaphase-promoting complex. We conclude that CCS52A1 participates in the endocycle onset by down-regulating CDKB1;1 activity through the destruction of CYCA2;3.




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