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运动细胞片状伪足中肌动蛋白依赖性逆向流动的分子机制。

Molecular mechanism of actin-dependent retrograde flow in lamellipodia of motile cells.

作者信息

Cramer L P

机构信息

The Randall Institute, Kings College London, 26-29 Drury Lane, London WC2B 5RL, UK.

出版信息

Front Biosci. 1997 Jun 1;2:d260-70. doi: 10.2741/a189.

DOI:10.2741/a189
PMID:9206973
Abstract

In motile, eukaryotic cells, a variety of cell-associated material (collectively termed here as 'particles') continuously flows, relative to the substratum, from the front to the back of the extreme margin of the cell (termed the 'lamellipodium'). This retrograde particle flow, occurs both over the surface of, and inside the lamellipodium. Force to drive retrograde particle flow in lamellipodia is dependent on actin filaments, but the precise mechanism of force generation, and function of the flow is generally not well understood. Actin filaments themselves, in lamellipodia of most motile cell types studied also flow retrograde relative to the substratum. This actin flow, in Aplysia bag cell neuronal growth cones, is known to be driven by activity of a myosin. In these growth cones, retrograde flow of cell surface-attached particles is coupled to retrograde actin flow. In Aplysia, force from retrograde actin flow may limit certain types of growth cone motility. In other motile cell types, such as keratocytes and fibroblasts, the mechanism of retrograde particle flow and function of retrograde actin flow in lamellipodia is poorly understood. For these cell types, recent data provide a basis for proposing alternative actin-based mechanisms to drive retrograde particle flow in lamellipodia. One mechanism is based on activity of a putative pointed end- directed actin motor, and the other on tension-driven surface lipid flow. Here I will review recent advances that have been made in determining the molecular mechanism of force generation to drive retrograde particle flow relative to the substratum in lamellipodia of motile cells. I will address the function of retrograde actin flow in lamellipodia, and apparent differences between Aplysia and other motile cell types.

摘要

在可运动的真核细胞中,各种与细胞相关的物质(在此统称为“颗粒”)相对于基质持续从细胞最边缘(称为“片状伪足”)的前端流向后端。这种逆行颗粒流在片状伪足的表面和内部均会发生。驱动片状伪足中逆行颗粒流的力依赖于肌动蛋白丝,但力产生的确切机制以及该流的功能通常尚未得到很好的理解。在大多数所研究的可运动细胞类型的片状伪足中,肌动蛋白丝本身相对于基质也会逆行流动。已知在海兔袋细胞神经元生长锥中,这种肌动蛋白流是由肌球蛋白的活性驱动的。在这些生长锥中,细胞表面附着颗粒的逆行流与肌动蛋白逆行流相耦合。在海兔中,来自肌动蛋白逆行流的力可能会限制某些类型的生长锥运动。在其他可运动细胞类型中,如角膜细胞和成纤维细胞,片状伪足中逆行颗粒流的机制以及肌动蛋白逆行流的功能了解甚少。对于这些细胞类型,最近的数据为提出驱动片状伪足中逆行颗粒流的基于肌动蛋白的替代机制提供了基础。一种机制基于一种假定的指向尖端的肌动蛋白马达的活性,另一种基于张力驱动的表面脂质流。在此,我将综述在确定驱动可运动细胞片状伪足中相对于基质逆行颗粒流的力产生分子机制方面所取得的最新进展。我将探讨片状伪足中肌动蛋白逆行流的功能,以及海兔与其他可运动细胞类型之间的明显差异。

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