RESEMBLANCE OF ACTIN-BINDING PROTEIN ACTIN GELS TO COVALENTLY CROSS-LINKED NETWORKS

RESEMBLANCE OF ACTIN-BINDING PROTEIN ACTIN GELS TO COVALENTLY CROSS-LINKED NETWORKS
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DOI:
10.1038/345089a0
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发表时间:
1990-05-03
期刊:
影响因子:
64.8
通讯作者:
STOSSEL, TP
STOSSEL, TP
中科院分区:
综合性期刊1区
文献类型:
--
作者:
JANMEY, PA;HVIDT, S;STOSSEL, TP

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细胞形状的维持通常是由于它们的表面弹性,这主要是由富含肌动蛋白的细胞质皮质引起的1,2。然而,在运动、吞噬或分裂时,这些细胞部分变成液体状。研究发现,可以与肌动蛋白结合并控制肌动蛋白丝的组装或交联的蛋白质,以及调节某些肌动蛋白结合蛋白活性的细胞内信息,表明这种“凝胶-溶胶”转化是由皮层富含肌动蛋白网络的重排引起的。另外,根据对肌动蛋白丝和棘阿米巴蛋白结合蛋白α-肌动蛋白混合物力学特性的研究,有人提出,这些转化可以通过肌动蛋白丝之间快速交换交联来解释4:当变形速率大于交联交换速率时,皮质网络将是固体的,但当变形速度慢到足以允许交联剂分子重新排列时,皮质网络将变形或“蠕变”。然而,在这里,我们报告,肌动蛋白丝和肌动蛋白结合蛋白(ABP)的混合物,许多高级真核生物的肌动蛋白交联蛋白,形成凝胶神学上等同于共价交联网络。这些凝胶在与大多数细胞表面运动相容的时间尺度上不会蠕变以响应施加的应力。这些发现支持了皮层细胞质动态力学特性背后更复杂和可控的机制,并可以解释为什么细胞在经常存在于组织中的恒定剪切力下不会崩溃。
THE maintainance of the shape of cells is often due to their surface elasticity, which arises mainly from an actin-rich cytoplasmic cortex1,2. On locomotion, phagocytosis or fission, however, these cells become partially fluid-like. The finding of proteins that can bind to actin and control the assembly of, or crosslink, actin filaments, and of intracellular messages that regulate the activities of some of these actin-binding proteins, indicates that such 'gel–sol' transformations result from the rearrangement of cortical actin-rich networks3. Alternatively, on the basis of a study of the mechanical properties of mixtures of actin filaments and anAcanthamoebaactin-binding protein, α-actinin, it has been proposed that these transformations can be accounted for by rapid exchange of crosslinks between actin filaments4: the cortical network would be solid when the deformation rate is greater than the rate of crosslink exchange, but would deform or 'creep' when deformation is slow enough to permit crosslinker molecules to rearrange. Here we report, however, that mixtures of actin filaments and actin-binding protein (ABP), an actin crosslinking protein of many higher eukaryotes, form gels Theologically equivalent to covalently crosslinked networks. These gels do not creep in response to applied stress on a time scale compatible with most cell-surface movements. These findings support a more complex and controlled mechanism underlying the dynamic mechanical properties of cortical cytoplasm, and can explain why cells do not collapse under the constant shear forces that often exist in tissues.