A link between mitotic entry and membrane growth suggests a novel model for cell size control
A link between mitotic entry and membrane growth suggests a novel model for cell size control
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DOI：
10.1083/jcb.201108108
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发表时间：
2012-04-02
影响因子：
7.8
通讯作者：
Kellogg, Douglas R.
中科院分区：
文献类型：
--
作者：
Anastasia, Steph D.;Duy Linh Nguyen;Kellogg, Douglas R.
通过膜运输向细胞表面添加新膜对于细胞生长是必需的。在本文中，我们报告说，通过Wee1依赖的抑制性磷酸化Cdk1阻断膜交通导致有丝分裂检查点逮捕。检查点信号由Rho1 GT3、蛋白激酶C（Pkc1）和蛋白磷酸酶2A（PP2A（Cdc55））的特定形式传递。通过这一途径的信号依赖于膜交通，并出现在极性芽生长过程中逐渐增加。我们假设，交付的小泡芽生长的网站产生的信号，是成比例的极化膜生长的程度和信号的强度是由下游组件读取，以确定何时发生足够的增长开始有丝分裂。生长依赖性信号可以解释膜生长如何与细胞周期进程相结合。它还可以控制细胞大小和形态发生，从而协调有丝分裂检查点功能的不同模型。
Addition of new membrane to the cell surface by membrane trafficking is necessary for cell growth. In this paper, we report that blocking membrane traffic causes a mitotic checkpoint arrest via Wee1-dependent inhibitory phosphorylation of Cdk1. Checkpoint signals are relayed by the Rho1 GTPase, protein kinase C (Pkc1), and a specific form of protein phosphatase 2A (PP2A(Cdc55)). Signaling via this pathway is dependent on membrane traffic and appears to increase gradually during polar bud growth. We hypothesize that delivery of vesicles to the site of bud growth generates a signal that is proportional to the extent of polarized membrane growth and that the strength of the signal is read by downstream components to determine when sufficient growth has occurred for initiation of mitosis. Growth-dependent signaling could explain how membrane growth is integrated with cell cycle progression. It could also control both cell size and morphogenesis, thereby reconciling divergent models for mitotic checkpoint function.