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

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.
Mesh Terms:
Arabidopsis Proteins, Cell Cycle, Cell Cycle Proteins, Cell Division, Cell Nucleus, Cyclin A, Cyclin A2, Cyclin-Dependent Kinases, Down-Regulation, Green Fluorescent Proteins, Protein Stability, Recombinant Fusion Proteins
Plant Physiol.
Date: Jul. 01, 2009
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