Instituto Gulbenkian de Ciência, Oeiras, Portugal.
J Cell Sci. 2012 Jul 1;125(Pt 13):3085-90. doi: 10.1242/jcs.097147. Epub 2012 Mar 27.
The completion of cytokinesis requires abscission of the midbody, a microtubule-rich cytoplasmic bridge that connects the daughter cells before their final separation. Although it has been established that both the midbody structure and membrane fusion are essential for abscission, the biochemical machinery and the cellular processes of abscission remain ill-defined. Here we report that human Mob1A and Mob1B proteins are involved in the regulation of abscission of the intercellular bridge. The Mob family is a group of highly conserved proteins in eukaryotes, described as binding partners as well as co-activators of protein kinases of the Ndr family, and as members of the Hippo pathway. We show that depletion of Mob1A and Mob1B by RNAi causes abscission failure as a consequence of hyper-stabilization of microtubules in the midbody region. Interestingly, depleting Mob1 also increases cell motility after cytokinesis, and induces prolonged centriole separation in G1 phase. In contrast, centrosomes fail to split when either Mob1A or Mob1B is overexpressed. Our findings indicate that human Mob1 proteins are involved in the regulation of microtubule stability at the midbody. We conclude that Mob1A and Mob1B are needed for cell abscission and centriole re-joining after telophase and cytokinesis.
胞质分裂的完成需要中体的分裂，中体是连接两个子细胞的富含微管的细胞质桥，在它们最终分离之前。尽管已经确定中体结构和膜融合对于分裂是必不可少的，但分裂的生化机制和细胞过程仍然不清楚。在这里，我们报告人类 Mob1A 和 Mob1B 蛋白参与调节细胞间桥的分裂。Mob 家族是真核生物中高度保守的一组蛋白，被描述为 Ndr 家族蛋白激酶的结合伴侣和共激活因子，以及 Hippo 途径的成员。我们发现，通过 RNAi 耗尽 Mob1A 和 Mob1B 会导致微管在中体区域过度稳定，从而导致分裂失败。有趣的是，耗尽 Mob1 还会增加胞质分裂后细胞的迁移能力，并诱导 G1 期中心粒分离时间延长。相比之下，当 Mob1A 或 Mob1B 过表达时，中心体无法分裂。我们的研究结果表明，人类 Mob1 蛋白参与调节中体微管的稳定性。我们得出结论，Mob1A 和 Mob1B 对于末期和胞质分裂后细胞的分裂和中心粒的重新连接是必需的。
