Temporal and spatial regulation of phosphoinositide signaling mediates cytokinesis
Temporal and spatial regulation of phosphoinositide signaling mediates cytokinesis
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DOI：
10.1016/j.devcel.2005.02.010
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发表时间：
2005-04-01
影响因子：
11.8
通讯作者：
Devreotes, P
中科院分区：
文献类型：
--
作者：
Janetopoulos, C;Borleis, J;Devreotes, P
极性是趋化性和胞质分裂的显著特征。在趋化性中，极性通过PI（3，4，5）P-3在细胞前缘的局部积累来建立，通过PI 3激酶和肿瘤抑制因子PTEN的时间和空间调节来实现。我们发现，随着D.当盘状突细胞变圆进入胞质分裂时，PI（3，4，5）P-3信号传导被均匀抑制。然后，随着纺锤体和细胞伸长，PI 3激酶和PTEN分别移动到两极和沟并在两极和沟发挥作用。缺乏这两种酶活性的细胞系不能调节PI（3，4，5）P-3水平，在胞质分裂中有缺陷，并且不能在悬浮液中分裂。细胞继续生长并复制其细胞核，产生大型多核细胞。不能进入细胞核之间的沟不能稳定地积累肌球蛋白丝或抑制肌动蛋白填充的皱褶。我们提出，磷酸肌醇连接的电路，类似于那些在细胞迁移过程中带来的不对称性，也调节胞质分裂的极性。
Polarity is a prominent feature of both chemotaxis and cytokinesis. In chemotaxis, polarity is established by local accumulation of PI(3,4,5)P-3 at the cell's leading edge, achieved through temporal and spatial regulation of PI3 kinases and the tumor suppressor, PTEN. We find that as migrating D. discoideum cells round up to enter cytokinesis, PI(3,4,5)P-3 signaling is uniformly suppressed. Then, as the spindle and cell elongate, PI3 kinases and PTEN move to and function at the poles and furrow, respectively. Cell lines lacking both of these enzymatic activities fail to modulate PI(3,4,5)P-3 levels, are defective in cytokinesis, and cannot divide in suspension. The cells continue to grow and duplicate their nuclei, generating large multinucleate cells. Furrows that fail to ingress between nuclei are unable to stably accumulate myosin filaments or suppress actin-filled ruffles. We propose that phosphoinositide-linked circuits, similar to those that bring about asymmetry during cell migration, also regulate polarity in cytokinesis.