NuMA is a component of an insoluble matrix at mitotic spindle poles

Citation
Ma. Dionne et al., NuMA is a component of an insoluble matrix at mitotic spindle poles, CELL MOTIL, 42(3), 1999, pp. 189-203
Citations number
87
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cell & Developmental Biology
Journal title
CELL MOTILITY AND THE CYTOSKELETON
ISSN journal
0886-1544 → ACNP
Volume
42
Issue
3
Year of publication
1999
Pages
189 - 203
Database
ISI
SICI code
0886-1544(1999)42:3<189:NIACOA>2.0.ZU;2-W
Abstract
NuMA associates with microtubule motors during mitosis to perform an essent ial role in organizing microtubule minus ends at spindle poles. Using immun ogold electron microscopy, we show that NuMA is a component of an electron- dense material concentrated at both mitotic spindle poles in PtK1 cells and the core of microtubule asters formed through a centrosome-independent mec hanism in cell-free mitotic extracts. This NuMA-containing material is dist inct from the peri-centriolar material and forms a matrix that appears to a nchor microtubule ends at the spindle pole. In stark contrast to convention al microtubule-associated proteins whose solubility is directly dependent o n microtubules, we find that once NuMA is incorporated into this matrix eit her in vivo or in vitro, it becomes insoluble and this insolubility is no l onger dependent on microtubules. NuMA is essential for the formation of thi s insoluble matrix at the core of mitotic asters assembled in vitro because the matrix is absent from mitotic asters assembled in a cell-free mitotic extract that is specifically depleted of NuMA. These physical properties ar e consistent with NuMA being a component of the putative mitotic spindle ma trix in vertebrate cells. Furthermore, given that NuMA is essential for spi ndle pole organization in vertebrate systems, it is likely that this insolu ble matrix plays an essential structural function in anchoring and/or stabi lizing microtubule minus ends at spindle poles in mitotic cells. Cell Motil . Cytoskeleton 42:189-203, 1999. (C) 1999 Wiley-Liss, Inc.