期刊
JOURNAL OF CELL BIOLOGY
卷 159, 期 4, 页码 589-599出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200208058
关键词
plus end-tracking proteins; p150(Glued); cytoskeleton; dynamics; mammalian cell culture
类别
资金
- NIGMS NIH HHS [GM 25062, R37 GM025062, R01 GM025062] Funding Source: Medline
The role of plus end-tracking proteins in regulating microtubule (MT) dynamics was investigated by expressing a dominant negative mutant that removed endogenous cytoplasmic linker proteins (CLIPs) from MT plus ends. In control CHO cells, MTs exhibited asymmetric behavior: MTs persistently grew toward the plasma membrane and displayed frequent fluctuations of length near the cell periphery. In the absence of CLIPs, the microtubule rescue frequency was reduced by sevenfold. MT behavior became symmetrical, consisting of persistent growth and persistent shortening. Removal of CLIPs also caused loss of p150(Glued) but not CLIP-associating protein (CLASP2) or EBI. This result raised the possibility that the change in dynamics was a result of the loss of either CLIPs or p150(Glued). To distinguish between these possibilities, we performed rescue experiments. Normal MT dynamics were restored by expression of the CLIP-170 head domain, but p150(Glued) was not recruited back to MT plus ends. Expression of p-150(Glued) head domain only partially restored MT dynamics. We conclude that the CLIP head domain is sufficient to alter MT dynamics either by itself serving as a rescue factor or indirectly by recruiting a rescue factor. By promoting a high rescue frequency, CLIPs provide a mechanism by which MT plus ends may be concentrated near the cell margin.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据