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机械化学信号传导维持了盘基网柄菌细胞的快速运动。

Mechano-chemical signaling maintains the rapid movement of Dictyostelium cells.

作者信息

Lombardi M L, Knecht D A, Lee J

机构信息

Department of Molecular and Cell Biology, University of Connecticut, Storrs, CT 06269, USA.

出版信息

Exp Cell Res. 2008 May 1;314(8):1850-9. doi: 10.1016/j.yexcr.2008.02.001. Epub 2008 Feb 14.

DOI:10.1016/j.yexcr.2008.02.001
PMID:18359017
Abstract

The survival of Dictyostelium cells depends on their ability to efficiently chemotax, either towards food or to form multicellular aggregates. Although the involvement of Ca2+ signaling during chemotaxis is well known, it is not clear how this regulates cell movement. Previously, fish epithelial keratocytes have been shown to display transient increases in intracellular calcium ([Ca2+]i) that are mediated by stretch-activated calcium channels (SACs), which play a role in retraction of the cell body [J. Lee, A. Ishihara, G. Oxford, B. Johnson, and K. Jacobson, Regulation of cell movement is mediated by stretch-activated calcium channels. Nature, 1999. 400(6742): p. 382-6.]. To investigate the involvement of SACs in Dictyostelium movement we performed high resolution calcium imaging in wild-type (NC4A2) Dictyostelium cells to detect changes in [Ca2+]i. We observed small, brief, Ca2+ transients in randomly moving wild-type cells that were dependent on both intracellular and extracellular sources of calcium. Treatment of cells with the SAC blocker gadolinium (Gd3+) inhibited transients and decreased cell speed, consistent with the involvement of SACs in regulating Dictyostelium motility. Additional support for SAC activity was given by the increase in frequency of Ca2+ transients when Dictyostelium cells were moving on a more adhesive substratum or when they were mechanically stretched. We conclude that mechano-chemical signaling via SACs plays a major role in maintaining the rapid movement of Dictyostelium cells.

摘要

盘基网柄菌细胞的存活取决于它们高效趋化的能力,这种趋化既可以是朝着食物,也可以是形成多细胞聚集体。尽管在趋化过程中Ca2+信号传导的参与是众所周知的,但尚不清楚它是如何调节细胞运动的。此前,已表明鱼类上皮角膜细胞会显示出细胞内钙([Ca2+]i)的短暂增加,这是由牵张激活钙通道(SACs)介导的,这些通道在细胞体回缩中起作用[J. 李、石原A、牛津G、约翰逊B和雅各布森K,细胞运动的调节由牵张激活钙通道介导。《自然》,1999年。400(6742): 第382 - 6页]。为了研究SACs在盘基网柄菌运动中的参与情况,我们在野生型(NC4A2)盘基网柄菌细胞中进行了高分辨率钙成像,以检测[Ca2+]i的变化。我们在随机移动的野生型细胞中观察到小的、短暂的Ca2+瞬变,这些瞬变依赖于细胞内和细胞外的钙源。用SAC阻断剂钆(Gd3+)处理细胞会抑制瞬变并降低细胞速度,这与SACs参与调节盘基网柄菌的运动性一致。当盘基网柄菌细胞在更具粘性的基质上移动或受到机械拉伸时,Ca2+瞬变频率的增加为SAC活性提供了额外的支持。我们得出结论,通过SACs的机械化学信号传导在维持盘基网柄菌细胞的快速运动中起主要作用。

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