Couchman J R, Lenn M, Rees D A
Eur J Cell Biol. 1985 Mar;36(2):182-94.
Using a chick cell phenotype specialised for locomotion with morphometric measurements made possible by modern instrumentation technology, we have reinvestigated motile functions in fibroblast locomotion. Quantitative analysis of rapid fluctuations in cell form and organelle distribution during locomotion showed many significant correlations between different parts of the cell despite much irregularity in individual displacements over the time scale of the order of one second. These broke down when external perturbations caused changes in shape or direction. Partial energy deprivation caused the cells to lose control of shape and organelle distribution even though forward protrusion continued unaffected. Cytoplasmic displacements shown by marker mitochondria correlated with adjacent fluctuations at the leading edge, and drug treatments which increased the amplitude of mitochondrial movements caused visible protrusions in projected positions at the leading edge. We conclude that fibroblast locomotion may be driven coordinately by a common set of motility mechanisms and that this coordination may be lost as a result of physical or pharmacological disturbance. Taking our evidence with results from other Laboratories, we propose the following cytoskeleton functions. (i) Protrusive activity, probably based on solation--gelation cycles of the actin based cytoskeleton and membrane recycling which provides cellular and membrane components for streaming through the cell body to the leading edge; this is Ca++ sensitive but relatively energy insensitive. (ii) Constraining activity on the cell membrane and on certain organelles to maintain shape and so facilitate directionality and the drawing along of the trailing body; this is Ca++ insensitive but relatively energy sensitive. (iii) Channeling function of microtubules to direct the flow towards multiple foci on the leading edge, and so determine cell polarity. Such a mechanism of locomotion for fibroblasts has many features consistent with evidence for other cell types, especially amoebae and leukocytes.
利用现代仪器技术实现的形态测量，对专门用于运动的鸡细胞表型进行研究，我们重新研究了成纤维细胞运动中的运动功能。对运动过程中细胞形态和细胞器分布的快速波动进行定量分析表明，尽管在大约一秒的时间尺度上个体位移存在很大的不规则性，但细胞不同部分之间仍存在许多显著的相关性。当外部扰动导致形状或方向发生变化时，这些相关性就会被打破。部分能量剥夺导致细胞失去对形状和细胞器分布的控制，即使向前突出仍不受影响。标记线粒体显示的细胞质位移与前沿相邻的波动相关，增加线粒体运动幅度的药物处理会在前缘的投影位置产生可见的突出。我们得出结论，成纤维细胞的运动可能由一组共同的运动机制协同驱动，并且这种协调可能会因物理或药理学干扰而丧失。结合我们的证据和其他实验室的结果，我们提出以下细胞骨架功能。（i）突出活动，可能基于肌动蛋白细胞骨架的溶胶 - 凝胶循环和膜循环，为通过细胞体流向前沿提供细胞和膜成分；这对Ca++敏感，但对能量相对不敏感。（ii）对细胞膜和某些细胞器的约束活动，以维持形状，从而促进方向性和拖尾体的牵拉；这对Ca++不敏感，但对能量相对敏感。（iii）微管的通道功能，将流动引导至前沿的多个焦点，从而确定细胞极性。这种成纤维细胞的运动机制具有许多与其他细胞类型（特别是变形虫和白细胞）的证据一致的特征。
