Gerisch Günther, Ecke Mary, Wischnewski Dirk, Schroth-Diez Britta
Max Planck Institute of Biochemistry, Am Klopferspitz 18, 82152 Martinsried, Germany.
BMC Cell Biol. 2011 Oct 7;12:42. doi: 10.1186/1471-2121-12-42.
In a motile polarized cell the actin system is differentiated to allow protrusion at the front and retraction at the tail. This differentiation is linked to the phosphoinositide pattern in the plasma membrane. In the highly motile Dictyostelium cells studied here, the front is dominated by PI3-kinases producing PI(3,4,5)tris-phosphate (PIP3), the tail by the PI3-phosphatase PTEN that hydrolyses PIP3 to PI(4,5)bis-phosphate. To study de-novo cell polarization, we first depolymerized actin and subsequently recorded the spontaneous reorganization of actin patterns in relation to PTEN.
In a transient stage of recovery from depolymerization, symmetric actin patterns alternate periodically with asymmetric ones. The switches to asymmetry coincide with the unilateral membrane-binding of PTEN. The modes of state transitions in the actin and PTEN systems differ. Transitions in the actin system propagate as waves that are initiated at single sites by the amplification of spontaneous fluctuations. In PTEN-null cells, these waves still propagate with normal speed but loose their regular periodicity. Membrane-binding of PTEN is induced at the border of a coherent PTEN-rich area in the form of expanding and regressing gradients.
The state transitions in actin organization and the reversible transition from cytoplasmic to membrane-bound PTEN are synchronized but their patterns differ. The transitions in actin organization are independent of PTEN, but when PTEN is present, they are coupled to periodic changes in the membrane-binding of this PIP3-degrading phosphatase. The PTEN oscillations are related to motility patterns of chemotaxing cells.
在一个运动性极化细胞中，肌动蛋白系统会发生分化，以允许细胞前端突出和后端回缩。这种分化与质膜中的磷酸肌醇模式相关。在本文研究的高度运动性的盘基网柄菌细胞中，前端主要由产生三磷酸磷脂酰肌醇（PI(3,4,5)P3）的PI3激酶主导，后端则由将PIP3水解为二磷酸磷脂酰肌醇（PI(4,5)P2）的PI3磷酸酶PTEN主导。为了研究细胞的重新极化，我们首先使肌动蛋白解聚，随后记录了肌动蛋白模式相对于PTEN的自发重组情况。
在从解聚中恢复的一个短暂阶段，对称的肌动蛋白模式与不对称的模式周期性交替出现。向不对称的转变与PTEN的单侧膜结合相吻合。肌动蛋白和PTEN系统中的状态转变模式不同。肌动蛋白系统中的转变以波的形式传播，这些波由自发波动的放大在单个位点引发。在PTEN缺失的细胞中，这些波仍以正常速度传播，但失去了其规则的周期性。PTEN的膜结合以扩展和消退梯度的形式在富含PTEN的连贯区域边界处被诱导。
肌动蛋白组织中的状态转变与PTEN从细胞质到膜结合的可逆转变是同步的，但它们的模式不同。肌动蛋白组织的转变独立于PTEN，但当PTEN存在时，它们与这种降解PIP3的磷酸酶的膜结合的周期性变化相关联。PTEN振荡与趋化细胞的运动模式相关。
