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  • 1
    Online Resource
    Online Resource
    Defects in Axonal Elongation and Neuronal Migration in Mice with Disrupted tau and map1b Genes
    Rockefeller University Press ; 2000
    In:  The Journal of Cell Biology Vol. 150, No. 5 ( 2000-09-04), p. 989-1000
    Details
    In: The Journal of Cell Biology, Rockefeller University Press, Vol. 150, No. 5 ( 2000-09-04), p. 989-1000
    Abstract: Tau and MAP1B are the main members of neuronal microtubule-associated proteins (MAPs), the functions of which have remained obscure because of a putative functional redundancy (Harada, A., K. Oguchi, S. Okabe, J. Kuno, S. Terada, T. Ohshima, R. Sato-Yoshitake, Y. Takei, T. Noda, and N. Hirokawa. 1994. Nature. 369:488–491; Takei, Y., S. Kondo, A. Harada, S. Inomata, T. Noda, and N. Hirokawa. 1997. J. Cell Biol. 137:1615–1626). To unmask the role of these proteins, we generated double-knockout mice with disrupted tau and map1b genes and compared their phenotypes with those of single-knockout mice. In the analysis of mice with a genetic background of predominantly C57Bl/6J, a hypoplastic commissural axon tract and disorganized neuronal layering were observed in the brains of the tau+/+map1b−/− mice. These phenotypes are markedly more severe in tau−/−map1b−/− double mutants, indicating that tau and MAP1B act in a synergistic fashion. Primary cultures of hippocampal neurons from tau−/−map1b−/− mice showed inhibited axonal elongation. In these cells, a generation of new axons via bundling of microtubules at the neck of the growth cones appeared to be disturbed. Cultured cerebellar neurons from tau−/−map1b−/− mice showed delayed neuronal migration concomitant with suppressed neurite elongation. These findings indicate the cooperative functions of tau and MAP1B in vivo in axonal elongation and neuronal migration as regulators of microtubule organization.
    Type of Medium: Online Resource
    ISSN: 0021-9525 , 1540-8140
    URL: Article
    DOI: 10.1083/jcb.150.5.989
    RVK:
    WA 15000
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 2000
    detail.hit.zdb_id: 1421310-2
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Delayed Development of Nervous System in Mice Homozygous for Disrupted Microtubule-associated Protein 1B (MAP1B) Gene
    Rockefeller University Press ; 1997
    In:  The Journal of Cell Biology Vol. 137, No. 7 ( 1997-06-30), p. 1615-1626
    Details
    In: The Journal of Cell Biology, Rockefeller University Press, Vol. 137, No. 7 ( 1997-06-30), p. 1615-1626
    Abstract: Microtubule-associated protein 1B (MAP1B), one of the microtubule-associated proteins (MAPs), is a major component of the neuronal cytoskeleton. It is expressed at high levels in immature neurons during growth of their axons, which indicates that it plays a crucial role in neuronal morphogenesis and neurite extension. To better define the role of MAP1B in vivo, we have used gene targeting to disrupt the murine MAP1B gene. Heterozygotes of our MAP1B disruption exhibit no overt abnormalities in their development and behavior, while homozygotes showed a slightly decreased brain weight and delayed nervous system development. Our data indicate that while MAP1B is not essential for survival, it is essential for normal time course development of the murine nervous system. These conclusions are very different from those of a previous MAP1B gene–targeting study (Edelmann, W., M. Zervas, P. Costello, L. Roback, I. Fischer, A. Hammarback, N. Cowan, P. Davis, B. Wainer, and R. Kucherlapati. 1996. Proc. Natl. Acad. Sci. USA. 93: 1270–1275). In this previous effort, homozygotes died before reaching 8-d embryos, while heterozygotes showed severely abnormal phenotypes in their nervous systems. Because the gene targeting event in these mice produced a gene encoding a 571–amino acid truncated product of MAP1B, it seems likely that the phenotypes seen arise from the truncated MAP1B product acting in a dominant-negative fashion, rather than a loss of MAP1B function.
    Type of Medium: Online Resource
    ISSN: 0021-9525 , 1540-8140
    URL: Article
    DOI: 10.1083/jcb.137.7.1615
    RVK:
    WA 15000
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 1997
    detail.hit.zdb_id: 1421310-2
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    MAP2 is required for dendrite elongation, PKA anchoring in dendrites, and proper PKA signal transduction
    Rockefeller University Press ; 2002
    In:  The Journal of Cell Biology Vol. 158, No. 3 ( 2002-08-05), p. 541-549
    Details
    In: The Journal of Cell Biology, Rockefeller University Press, Vol. 158, No. 3 ( 2002-08-05), p. 541-549
    Abstract: Microtubule-associated protein 2 (MAP2) is a major component of cross-bridges between microtubules in dendrites, and is known to stabilize microtubules. MAP2 also has a binding domain for the regulatory subunit II of cAMP-dependent protein kinase (PKA). We found that there is reduction in microtubule density in dendrites and a reduction of dendritic length in MAP2-deficient mice. Moreover, there is a significant reduction of various subunits of PKA in dendrites and total amounts of various PKA subunits in hippocampal tissue and cultured neurons. In MAP2-deficient cultured neurons, the induction rate of phosphorylated CREB after forskolin stimulation was much lower than in wild-type neurons. Therefore, MAP2 is an anchoring protein of PKA in dendrites, whose loss leads to reduced amount of dendritic and total PKA and reduced activation of CREB.
    Type of Medium: Online Resource
    ISSN: 1540-8140 , 0021-9525
    URL: Article
    DOI: 10.1083/jcb.200110134
    RVK:
    WA 15000
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 2002
    detail.hit.zdb_id: 1421310-2
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    DOCK5 functions as a key signaling adaptor that links FcεRI signals to microtubule dynamics during mast cell degranulation
    Rockefeller University Press ; 2014
    In:  The Journal of Cell Biology Vol. 205, No. 6 ( 2014-06-23), p. 2056OIA110-
    Details
    In: The Journal of Cell Biology, Rockefeller University Press, Vol. 205, No. 6 ( 2014-06-23), p. 2056OIA110-
    Type of Medium: Online Resource
    ISSN: 0021-9525 , 1540-8140
    URL: Article
    DOI: 10.1083/jcb.2056OIA110
    RVK:
    WA 15000
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 2014
    detail.hit.zdb_id: 1421310-2
    SSG: 12
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  • 5
    Online Resource
    Online Resource
    DOCK5 functions as a key signaling adaptor that links FcεRI signals to microtubule dynamics during mast cell degranulation
    Rockefeller University Press ; 2014
    In:  Journal of Experimental Medicine Vol. 211, No. 7 ( 2014-06-30), p. 1407-1419
    Details
    In: Journal of Experimental Medicine, Rockefeller University Press, Vol. 211, No. 7 ( 2014-06-30), p. 1407-1419
    Abstract: Mast cells play a key role in the induction of anaphylaxis, a life-threatening IgE-dependent allergic reaction, by secreting chemical mediators that are stored in secretory granules. Degranulation of mast cells is triggered by aggregation of the high-affinity IgE receptor, FcεRI, and involves dynamic rearrangement of microtubules. Although much is known about proximal signals downstream of FcεRI, the distal signaling events controlling microtubule dynamics remain elusive. Here we report that DOCK5, an atypical guanine nucleotide exchange factor (GEF) for Rac, is essential for mast cell degranulation. As such, we found that DOCK5-deficient mice exhibit resistance to systemic and cutaneous anaphylaxis. The Rac GEF activity of DOCK5 is surprisingly not required for mast cell degranulation. Instead, DOCK5 associated with Nck2 and Akt to regulate microtubule dynamics through phosphorylation and inactivation of GSK3β. When DOCK5–Nck2–Akt interactions were disrupted, microtubule formation and degranulation response were severely impaired. Our results thus identify DOCK5 as a key signaling adaptor that orchestrates remodeling of the microtubule network essential for mast cell degranulation.
    Type of Medium: Online Resource
    ISSN: 1540-9538 , 0022-1007
    URL: Article
    DOI: 10.1084/jem.20131926
    RVK:
    XA 10000
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 2014
    detail.hit.zdb_id: 1477240-1
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  • 6
    Online Resource
    Online Resource
    Synergistic effects of MAP2 and MAP1B knockout in neuronal migration, dendritic outgrowth, and microtubule organization
    Rockefeller University Press ; 2001
    In:  The Journal of Cell Biology Vol. 155, No. 1 ( 2001-10-01), p. 65-76
    Details
    In: The Journal of Cell Biology, Rockefeller University Press, Vol. 155, No. 1 ( 2001-10-01), p. 65-76
    Abstract: MAP1B and MAP2 are major members of neuronal microtubule-associated proteins (MAPs). To gain insights into the function of MAP2 in vivo, we generated MAP2-deficient (map2−/−) mice. They developed without any apparent abnormalities, which indicates that MAP2 is dispensable in mouse survival. Because previous reports suggest a functional redundancy among MAPs, we next generated mice lacking both MAP2 and MAP1B to test their possible synergistic functions in vivo. Map2−/−map1b−/− mice died in their perinatal period. They showed not only fiber tract malformations but also disrupted cortical patterning caused by retarded neuronal migration. In spite of this, their cortical layer maintained an “inside-out” pattern. Detailed observation of primary cultures of hippocampal neurons from map2−/−map1b−/− mice revealed inhibited microtubule bundling and neurite elongation. In these neurons, synergistic effects caused by the loss of MAP2 and MAP1B were more apparent in dendrites than in axons. The spacing of microtubules was reduced significantly in map2−/−map1b−/− mice in vitro and in vivo. These results suggest that MAP2 and MAP1B have overlapping functions in neuronal migration and neurite outgrowth by organizing microtubules in developing neurons both for axonal and dendritic morphogenesis but more dominantly for dendritic morphogenesis.
    Type of Medium: Online Resource
    ISSN: 1540-8140 , 0021-9525
    URL: Article
    DOI: 10.1083/jcb.200106025
    RVK:
    WA 15000
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 2001
    detail.hit.zdb_id: 1421310-2
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    Defect in Synaptic Vesicle Precursor Transport and Neuronal Cell Death in KIF1A Motor Protein–deficient Mice
    Rockefeller University Press ; 1998
    In:  The Journal of Cell Biology Vol. 141, No. 2 ( 1998-04-20), p. 431-441
    Details
    In: The Journal of Cell Biology, Rockefeller University Press, Vol. 141, No. 2 ( 1998-04-20), p. 431-441
    Abstract: The nerve axon is a good model system for studying the molecular mechanism of organelle transport in cells. Recently, the new kinesin superfamily proteins (KIFs) have been identified as candidate motor proteins involved in organelle transport. Among them KIF1A, a murine homologue of unc-104 gene of Caenorhabditis elegans, is a unique monomeric neuron– specific microtubule plus end–directed motor and has been proposed as a transporter of synaptic vesicle precursors (Okada, Y., H. Yamazaki, Y. Sekine-Aizawa, and N. Hirokawa. 1995. Cell. 81:769–780). To elucidate the function of KIF1A in vivo, we disrupted the KIF1A gene in mice. KIF1A mutants died mostly within a day after birth showing motor and sensory disturbances. In the nervous systems of these mutants, the transport of synaptic vesicle precursors showed a specific and significant decrease. Consequently, synaptic vesicle density decreased dramatically, and clusters of clear small vesicles accumulated in the cell bodies. Furthermore, marked neuronal degeneration and death occurred both in KIF1A mutant mice and in cultures of mutant neurons. The neuronal death in cultures was blocked by coculture with wild-type neurons or exposure to a low concentration of glutamate. These results in cultures suggested that the mutant neurons might not sufficiently receive afferent stimulation, such as neuronal contacts or neurotransmission, resulting in cell death. Thus, our results demonstrate that KIF1A transports a synaptic vesicle precursor and that KIF1A-mediated axonal transport plays a critical role in viability, maintenance, and function of neurons, particularly mature neurons.
    Type of Medium: Online Resource
    ISSN: 0021-9525 , 1540-8140
    URL: Article
    DOI: 10.1083/jcb.141.2.431
    RVK:
    WA 15000
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 1998
    detail.hit.zdb_id: 1421310-2
    SSG: 12
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