Cell contraction caused by microtubule disruption is accompanied by shape changes and an increased elasticity measured by scanning acoustic microscopy
Cell contraction caused by microtubule disruption is accompanied by shape changes and an increased elasticity measured by scanning acoustic microscopy
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DOI：
10.1007/bf02737896
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发表时间：
1998-01-01
影响因子：
2.6
通讯作者：
Bereiter-Hahn, Juergen
中科院分区：
文献类型：
--
作者：
Karl, Ilonka;Bereiter-Hahn, Juergen
微丝的交联状态和肌球蛋白驱动的收缩状态是膜下细胞皮质力学性能的主要决定因素，这对细胞的成形机制具有重要意义。因此，肌动球蛋白网络收缩状态的任何变化都会改变其力学性能，最终导致形状变化。微管与细胞机械性能之间的关系尚不清楚。主要的问题出现是因为微管的破坏增强了acto myosin驱动的收缩。这一反应及其对细胞形态和弹性的影响已经在单个Xth-2细胞中进行了研究。用聚合抑制剂Colcemid诱导微管破裂。这种反应是双相的：细胞形状从煎蛋状转变为凸起的表面形貌，伴随着细胞质弹性硬度的增加，通过扫描声学显微镜测量纵向声速。细胞周边部弹性增加，30min后达到峰值。随后，当细胞质从外围回缩时，纵向声速(弹性)降低。同时，在密集培养中，F-肌动蛋白和应力纤维从细胞中心到细胞连接的应力纤维增加了两到三倍，这可能是张力增加的结果。
The state of crosslinking of microfilaments and the state of myosin-driven contraction are the main determinants of the mechanical properties of the cell cortex underneath the membrane, which is significant for the mechanism of shaping cells. Therefore, any change in the contractile state of the actomyosin network would alter the mechanical properties and finally result in shape changes. The relationship of microtubules to the mechanical properties of cells is still obscure. The main problem arises because disruption of microtubules enhances acto-myosin-driven contraction. This reaction and its impact on cell shape and elasticity have been investigated in single XTH-2 cells. Microtubule disruption was induced by colcemid, a polymerization inhibitor. The reaction was biphasic: a change in cell shape from a fried egg shape to a convex surface topography was accompanied by an increase in elastic stiffness of the cytoplasm, measured as longitudinal sound velocity revealed by scanning acoustic microscope. Elasticity increases in the cell periphery and reaches its peak after 30 min. Subsequently while the cytoplasm retracts from the periphery, longitudinal sound velocity (elasticity) decreases. Simultaneously, a two- to threefold increase of F-actin and alignment of stress fibers from the cell center to cell-cell junctions in dense cultures are induced, supposedly a consequence of the increased tension.