Biogenesis of N-cadherin-dependent cell-cell contacts in living fibroblasts is a microtubule-dependent kinesin-driven mechanism

被引:121
作者
Mary, S [1 ]
Charrasse, S [1 ]
Meriane, M [1 ]
Comunale, F [1 ]
Travo, P [1 ]
Blangy, A [1 ]
Gauthier-Rouvière, C [1 ]
机构
[1] CNRS, UPR 1086, Ctr Rech Biochim Macromol, F-34293 Montpellier, France
关键词
D O I
10.1091/mbc.01-07-0337
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Cadherin-mediated cell-cell adhesion is a dynamic process that is regulated during embryonic development, cell migration, and differentiation. Different cadherins are expressed in specific tissues consistent with their roles in cell type recognition. In this study, we examine the formation of N-cadherin-dependent cell-cell contacts in fibroblasts and myoblasts. In contrast to E-cadherin, both endogenous and ectopically expressed N-cadherin shuttles between an intracellular and a plasma membrane pool. Initial formation of N-cadherin-dependent cell-cell contacts results from the recruitment of the intracellular pool of N-cadherin to the plasma membrane. N-cadherin also localizes to the Golgi apparatus and both secretory and endocytotic vesicles. We demonstrate that the intracellular pool of N-cadherin is tightly associated with the microtubule (MT) network and that junction formation requires MTs. In addition, localization of N-cadherin to the cortex is dependent on an intact F-actin cytoskeleton. We show that N-cadherin transport requires the MT network as well as the activity of the MT-associated motor kinesin. In conclusion, we propose that N-cadherin distribution is a regulated process promoted by cell-cell contact formation, which controls the biogenesis and turnover of the junctions through the MT network.
引用
收藏
页码:285 / 301
页数:17
相关论文
共 41 条
[1]   Quantitative analysis of cadherin-catenin-actin reorganization during development of cell-cell adhesion [J].
Adams, CL ;
Nelson, WJ ;
Smith, SJ .
JOURNAL OF CELL BIOLOGY, 1996, 135 (06) :1899-1911
[2]   EXPRESSION OF CELL-ADHESION MOLECULES DURING INITIATION AND CESSATION OF NEURAL CREST CELL-MIGRATION [J].
AKITAYA, T ;
BRONNERFRASER, M .
DEVELOPMENTAL DYNAMICS, 1992, 194 (01) :12-20
[3]   A MONOCLONAL-ANTIBODY AGAINST KINESIN INHIBITS BOTH ANTEROGRADE AND RETROGRADE FAST AXONAL-TRANSPORT IN SQUID AXOPLASM [J].
BRADY, ST ;
PFISTER, KK ;
BLOOM, GS .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1990, 87 (03) :1061-1065
[4]   MECHANISMS OF NEURAL CREST CELL-MIGRATION [J].
BRONNERFRASER, M .
BIOESSAYS, 1993, 15 (04) :221-230
[5]  
Charrasse S, 1998, J CELL SCI, V111, P1371
[6]   Cadherin-mediated regulation of microtubule dynamics [J].
Chausovsky, A ;
Bershadsky, AD ;
Borisy, GG .
NATURE CELL BIOLOGY, 2000, 2 (11) :797-804
[7]   Golgi dispersal during microtubule disruption: Regeneration of Golgi stacks at peripheral endoplasmic reticulum exit sites [J].
Cole, NB ;
Sciaky, N ;
Marotta, A ;
Song, J ;
LippincottSchwartz, J .
MOLECULAR BIOLOGY OF THE CELL, 1996, 7 (04) :631-650
[8]   Tumor necrosis factor induces hyperphosphorylation of kinesin light chain and inhibits kinesin-mediated transport of mitochondria [J].
De Vos, K ;
Severin, F ;
Van Herreweghe, F ;
Vancompernolle, K ;
Goossens, V ;
Hyman, A ;
Grooten, J .
JOURNAL OF CELL BIOLOGY, 2000, 149 (06) :1207-1214
[9]   RhoG GTPase controls a pathway that independently activates Rac1 and Cdc42Hs [J].
Gauthier-Rouvière, C ;
Vignal, E ;
Mériane, M ;
Roux, P ;
Montcourier, P ;
Fort, P .
MOLECULAR BIOLOGY OF THE CELL, 1998, 9 (06) :1379-1394
[10]   Regulation of cadherin adhesive activity [J].
Gumbiner, BM .
JOURNAL OF CELL BIOLOGY, 2000, 148 (03) :399-403