CDKB1;1 Forms a Functional Complex with CYCA2;3 to Suppress Endocycle Onset
CDKB1;1 Forms a Functional Complex with CYCA2;3 to Suppress Endocycle Onset
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DOI：
10.1104/pp.109.140269
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发表时间：
2009-07-01
期刊：
影响因子：
7.4
通讯作者：
De Veylder, Lieven
中科院分区：
文献类型：
--
作者：
Boudolf, Veronique;Lammens, Tim;De Veylder, Lieven
有丝分裂到内循环的转变需要M期相关的细胞周期蛋白依赖性激酶（CDK）活性的受控失活。以前，B型CDKB 1;1被确定为内循环启动的重要负调节因子。在这里，我们表明，CDKB 1;1 copurifies和协会与A2型细胞周期蛋白CYCA 2;3。CYCA 2;3与CDKB 1;1的共表达触发了异位细胞分裂并抑制了核内复制。此外，CDKB 1;1的显性负性等位基因过表达后观察到的增强的核内复制表型可以通过CYCA 2;3共过表达部分补充，说明两个亚基在体内结合形成功能复合物。CYCA 2;3蛋白的稳定性被发现是由CCS 52 A1，一种后期促进复合物的激活剂控制的。我们的结论是，CCS 52 A1通过破坏CYCA 2;3下调CDKB 1;1活性参与内循环启动。
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.