Journal
PLANT PHYSIOLOGY
Volume 150, Issue 3, Pages 1482-1493Publisher
AMER SOC PLANT BIOLOGISTS
DOI: 10.1104/pp.109.140269
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Funding
- Interuniversity Attraction Poles Program [VI/33]
- Belgian State, Science Policy Office
- Institute for the Promotion and Innovation through Science and Technology [20193, 20176]
- Research Foundation-Flanders [G008306]
- European Union Human Resources and Mobility [MESTCT2004514632]
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The mitosis-to-endocycle transition requires the controlled inactivation of M phase-associated cyclin-dependent kinase (CDK) activity. Previously, the B-type CDKB1;1 was identified as an important negative regulator of endocycle onset. Here, we demonstrate that CDKB1;1 copurifies and associates with the A2-type cyclin CYCA2;3. Coexpression 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 endocycle onset by down-regulating CDKB1;1 activity through the destruction of CYCA2;3.
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