Intermediate filaments are dynamic and motile elements of cellular architecture

被引:200
作者
Helfand, BT [1 ]
Chang, L [1 ]
Goldman, RD [1 ]
机构
[1] Northwestern Univ, Dept Cell & Mol Biol, Feinberg Sch Med, Chicago, IL 60611 USA
关键词
vimentin; neurofilaments; keratin; intermediate filaments;
D O I
10.1242/jcs.00936
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Recent evidence showing that intermediate filaments (IFs) are dynamic, motile elements of the cytoskeletal. repertoire of vertebrate cells has overturned the long-standing view that they simply form static 'space filling' cytoplasmic networks. In fact, many types of IF are now known to engage in a remarkable array of movements that are closely associated with their assembly, disassembly and subcellular organization. Some of these motile properties are intrinsic to IFs and others are attributable to molecular crosstalk with either microtubules or actin-containing microfilaments. This crosstalk is, to a large extent, mediated by molecular motors, including conventional kinesin and cytoplasmic dynein. These motors are responsible for the high-speed delivery of nonfilamentous IF precursors and short filaments to specific regions of the cytoplasm, where they assemble into long IFs. Interestingly, the patterns and speeds of IF movements vary in different cell types and even within different regions of the same cell. These differences in motility may be related to their interactions with different types of molecular motor and/or other factors, such as IF-associated proteins.
引用
收藏
页码:133 / 141
页数:9
相关论文
共 92 条
  • [1] Neurofilament heavy chain side arm phosphorylation regulates axonal transport of neurofilaments
    Ackerley, S
    Thornhill, P
    Grierson, AJ
    Brownlees, J
    Anderton, BH
    Leigh, PN
    Shaw, CE
    Miller, CCJ
    [J]. JOURNAL OF CELL BIOLOGY, 2003, 161 (03) : 489 - 495
  • [2] Deletions of the heavy neurofilament subunit tail in amyotrophic lateral sclerosis
    Al-Chalabi, A
    Andersen, PM
    Nilsson, P
    Chioza, B
    Andersson, JL
    Russ, C
    Shaw, CE
    Powell, JF
    Leigh, PN
    [J]. HUMAN MOLECULAR GENETICS, 1999, 8 (02) : 157 - 164
  • [3] Neurofilaments and neurological disease
    Al-Chalabi, A
    Miller, CCJ
    [J]. BIOESSAYS, 2003, 25 (04) : 346 - 355
  • [4] Quick guide - Dynactin
    Allan, V
    [J]. CURRENT BIOLOGY, 2000, 10 (12) : R432 - R432
  • [5] AVSYUK AV, 1995, DOKL AKAD NAUK, V345, P644
  • [6] FAST AXONAL-TRANSPORT IN AMYOTROPHIC-LATERAL-SCLEROSIS - AN INTRAAXONAL ORGANELLE TRAFFIC ANALYSIS
    BREUER, AC
    LYNN, MP
    ATKINSON, MB
    CHOU, SM
    WILBOURN, AJ
    MARKS, KE
    CULVER, JE
    FLEEGLER, EJ
    [J]. NEUROLOGY, 1987, 37 (05) : 738 - 748
  • [7] FAST AXONAL-TRANSPORT ALTERATIONS IN AMYOTROPHIC LATERAL SCLEROSIS (ALS) AND IN PARATHYROID-HORMONE (PTH)-TREATED AXONS
    BREUER, AC
    ATKINSON, MB
    [J]. CELL MOTILITY AND THE CYTOSKELETON, 1988, 10 (1-2): : 321 - 330
  • [8] Slow axonal transport: stop and go traffic in the axon
    Brown, A
    [J]. NATURE REVIEWS MOLECULAR CELL BIOLOGY, 2000, 1 (02) : 153 - 156
  • [9] Charcot-Marie-Tooth disease neurofilament mutations disrupt neurofilament assembly and axonal transport
    Brownlees, J
    Ackerley, S
    Grierson, AJ
    Jacobsen, NJO
    Shea, K
    Anderton, BH
    Leigh, PN
    Shaw, CE
    Miller, CCJ
    [J]. HUMAN MOLECULAR GENETICS, 2002, 11 (23) : 2837 - 2844
  • [10] Overexpression of the dynamitin (p50) subunit of the dynactin complex disrupts dynein-dependent maintenance of membrane organelle distribution
    Burkhardt, JK
    Echeverri, CJ
    Nilsson, T
    Vallee, RB
    [J]. JOURNAL OF CELL BIOLOGY, 1997, 139 (02) : 469 - 484