Aurora B and cyclin B have opposite effects on the timing of cytokinesis abscission in Drosophila germ cells and in vertebrate somatic cells.

Aurora B and cyclin B have opposite effects on the timing of cytokinesis abscission in Drosophila germ cells and in vertebrate somatic cells.
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DOI:
10.1016/j.devcel.2013.07.005
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发表时间:
2013-08-12
期刊:
影响因子:
11.8
通讯作者:
Huynh JR
Huynh JR
中科院分区:
生物学1区
文献类型:
--
作者:
Mathieu J;Cauvin C;Moch C;Radford SJ;Sampaio P;Perdigoto CN;Schweisguth F;Bardin AJ;Sunkel CE;McKim K;Echard A;Huynh JR

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脱落是胞质分裂的最后一步,物理上分离姐妹细胞的细胞质。作为细胞分裂的最后阶段,在动物发育过程中,脱落的特征很少。在这里,我们发现 Aurora B 和 Survivin 通过抑制分化过程中的脱落来调节每个果蝇卵室中生殖细胞的数量。这种抑制作用是由 Cyclin B 的 Aurora B 依赖性磷酸化介导的,因为 Cyclin B 的磷模拟形式可以挽救 Aurora B 功能丧失引起的过早脱落。我们发现 Cyclin B 定位于胞质分裂桥,在那里促进脱落。我们提出 Aurora-B 和 Cyclin-B 之间的相互抑制调节脱落的持续时间,从而调节每个囊肿中姐妹细胞的数量。最后,我们发现,抑制脊椎动物细胞中的 Aurora B 和 Cdk-1 活性也对脱落时间产生相反的影响,表明这些机制可能存在保守性。
Abscission is the last step of cytokinesis that physically separates the cytoplasm of sister cells. As the final stage of cell division, abscission is poorly characterized during animal development. Here, we show that Aurora B and Survivin regulate the number of germ cells in each Drosophila egg chamber by inhibiting abscission during differentiation. This inhibition is mediated by an Aurora B-dependent phosphorylation of Cyclin B, as a phosphomimic form of Cyclin B rescues premature abscission caused by a loss-of-function of Aurora B. We show that Cyclin B localizes at the cytokinesis bridge, where it promotes abscission. We propose that mutual inhibitions between Aurora-B and Cyclin-B regulate the duration of abscission and thereby the number of sister cells in each cyst. Finally, we show that inhibitions of Aurora B and Cdk-1 activity in vertebrate cells also have opposite effects on the timing of abscission, suggesting a possible conservation of these mechanisms.
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