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  1. Article ; Online: Inositol 1,4,5-Trisphosphate Receptor Type 3 Regulates Neuronal Growth Cone Sensitivity to Guidance Signals

    Carmen Chan / Noriko Ooashi / Hiroki Akiyama / Tetsuko Fukuda / Mariko Inoue / Toru Matsu-ura / Tomomi Shimogori / Katsuhiko Mikoshiba / Hiroyuki Kamiguchi

    iScience, Vol 23, Iss 3, Pp - (2020)

    2020  

    Abstract: Summary: During neurodevelopment, the growth cone deciphers directional information from extracellular guidance cues presented as shallow concentration gradients via signal amplification. However, it remains unclear how the growth cone controls this ... ...

    Abstract Summary: During neurodevelopment, the growth cone deciphers directional information from extracellular guidance cues presented as shallow concentration gradients via signal amplification. However, it remains unclear how the growth cone controls this amplification process during its navigation through an environment in which basal cue concentrations vary widely. Here, we identified inositol 1,4,5-trisphosphate (IP3) receptor type 3 as a regulator of axonal sensitivity to guidance cues in vitro and in vivo. Growth cones lacking the type 3 subunit are hypersensitive to nerve growth factor (NGF), an IP3-dependent attractive cue, and incapable of turning toward normal concentration ranges of NGF to which wild-type growth cones respond. This is due to globally, but not asymmetrically, activated Ca2+ signaling in the hypersensitive growth cones. Remarkably, lower NGF concentrations can polarize growth cones for turning if IP3 receptor type 3 is deficient. These data suggest a subtype-specific IP3 receptor function in sensitivity adjustment during axon navigation. : Biological Sciences; Neuroscience; Molecular Neuroscience; Cellular Neuroscience Subject Areas: Biological Sciences, Neuroscience, Molecular Neuroscience, Cellular Neuroscience
    Keywords Science ; Q
    Subject code 612
    Language English
    Publishing date 2020-03-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Myosin Va and Endoplasmic Reticulum Calcium Channel Complex Regulates Membrane Export during Axon Guidance

    Fumitaka Wada / Asuka Nakata / Yoshiro Tatsu / Noriko Ooashi / Tetsuko Fukuda / Takuji Nabetani / Hiroyuki Kamiguchi

    Cell Reports, Vol 15, Iss 6, Pp 1329-

    2016  Volume 1344

    Abstract: During axon guidance, growth cones navigate toward attractive cues by inserting new membrane on the cue side. This process depends on Ca2+ release from endoplasmic reticulum (ER) Ca2+ channels, but the Ca2+ sensor and effector governing this asymmetric ... ...

    Abstract During axon guidance, growth cones navigate toward attractive cues by inserting new membrane on the cue side. This process depends on Ca2+ release from endoplasmic reticulum (ER) Ca2+ channels, but the Ca2+ sensor and effector governing this asymmetric vesicle export remain unknown. We identified a protein complex that controls asymmetric ER Ca2+-dependent membrane vesicle export. The Ca2+-dependent motor protein myosin Va (MyoVa) tethers membrane vesicles to the ER via a common binding site on the two major ER Ca2+ channels, inositol 1,4,5-trisphosphate and ryanodine receptors. In response to attractive cues, micromolar Ca2+ from ER channels triggers MyoVa-channel dissociation and the movement of freed vesicles to the cue side, enabling growth cone turning. MyoVa-Ca2+ channel interactions are required for proper long-range axon growth in developing spinal cord in vivo. These findings reveal a peri-ER membrane export pathway for Ca2+-dependent attraction in axon guidance.
    Keywords Biology (General) ; QH301-705.5
    Language English
    Publishing date 2016-05-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Hyperactive and impulsive behaviors of LMTK1 knockout mice

    Miyuki Takahashi / Arika Sugiyama / Ran Wei / Shizuka Kobayashi / Kimiko Fukuda / Hironori Nishino / Roka Takahashi / Koji Tsutsumi / Ichiro Kita / Kanae Ando / Toshiya Manabe / Hiroyuki Kamiguchi / Mineko Tomomura / Shin-ichi Hisanaga

    Scientific Reports, Vol 10, Iss 1, Pp 1-

    2020  Volume 13

    Abstract: Abstract Lemur tail kinase 1 (LMTK1), previously called Apoptosis-Associated Tyrosine Kinase (AATYK), remains an uncharacterized Ser/Thr protein kinase that is predominantly expressed in the brain. It is recently reported that LMTK1A, an isoform of LMTK1, ...

    Abstract Abstract Lemur tail kinase 1 (LMTK1), previously called Apoptosis-Associated Tyrosine Kinase (AATYK), remains an uncharacterized Ser/Thr protein kinase that is predominantly expressed in the brain. It is recently reported that LMTK1A, an isoform of LMTK1, binds to recycling endosomes through its palmitoylation and regulates endosomal trafficking by suppressing the activity of Rab11 small GTPase. In neurons, knockdown or knockout of LMTK1 results in longer axons, greater branching of dendrites and increased number of spines, suggesting that LMTK1 plays a role in neuronal circuit formation. However, its in vivo function remained to be investigated. Here, we examined the brain structures and behaviors of LMTK1 knockout (KO) mice. LMTK1 was expressed in most neurons throughout the brain. The overall brain structure appeared to be normal in LMTK1 KO mice, but the numbers of synapses were increased. LMTK1 KO mice had a slight impairment in memory formation and exhibited distinct psychiatric behaviors such as hyperactivity, impulsiveness and high motor coordination without social interaction deficits. Some of these abnormal behaviors represent core features of attention deficit hyperactive disorder (ADHD), suggesting the possible involvement of LMTK1 in the pathogenesis of ADHD.
    Keywords Medicine ; R ; Science ; Q
    Subject code 572
    Language English
    Publishing date 2020-09-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Reversal of axonal growth defects in an extraocular fibrosis model by engineering the kinesin–microtubule interface

    Itsushi Minoura / Hiroko Takazaki / Rie Ayukawa / Chihiro Saruta / You Hachikubo / Seiichi Uchimura / Tomonobu Hida / Hiroyuki Kamiguchi / Tomomi Shimogori / Etsuko Muto

    Nature Communications, Vol 7, Iss 1, Pp 1-

    2016  Volume 11

    Abstract: How mutations in β3-tubulin cause axonal growth defects in congenital fibrosis of the extraocular muscles type 3 remains elusive. Minoura et al. develop a model system using recombinant human tubulin that demonstrates a link between tubulin mutation, ... ...

    Abstract How mutations in β3-tubulin cause axonal growth defects in congenital fibrosis of the extraocular muscles type 3 remains elusive. Minoura et al. develop a model system using recombinant human tubulin that demonstrates a link between tubulin mutation, impaired kinesin motility and axonal growth defects.
    Keywords Science ; Q
    Language English
    Publishing date 2016-01-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: GTP hydrolysis of TC10 promotes neurite outgrowth through exocytic fusion of Rab11- and L1-containing vesicles by releasing exocyst component Exo70.

    Akane Fujita / Shingo Koinuma / Sayaka Yasuda / Hiroyuki Nagai / Hiroyuki Kamiguchi / Naoyuki Wada / Takeshi Nakamura

    PLoS ONE, Vol 8, Iss 11, p e

    2013  Volume 79689

    Abstract: The use of exocytosis for membrane expansion at nerve growth cones is critical for neurite outgrowth. TC10 is a Rho family GTPase that is essential for specific types of vesicular trafficking to the plasma membrane. Recent studies have shown that TC10 ... ...

    Abstract The use of exocytosis for membrane expansion at nerve growth cones is critical for neurite outgrowth. TC10 is a Rho family GTPase that is essential for specific types of vesicular trafficking to the plasma membrane. Recent studies have shown that TC10 and its effector Exo70, a component of the exocyst tethering complex, contribute to neurite outgrowth. However, the molecular mechanisms of the neuritogenesis-promoting functions of TC10 remain to be established. Here, we propose that GTP hydrolysis of vesicular TC10 near the plasma membrane promotes neurite outgrowth by accelerating vesicle fusion by releasing Exo70. Using Förster resonance energy transfer (FRET)-based biosensors, we show that TC10 activity at the plasma membrane decreased at extending growth cones in hippocampal neurons and nerve growth factor (NGF)-treated PC12 cells. In neuronal cells, TC10 activity at vesicles was higher than its activity at the plasma membrane, and TC10-positive vesicles were found to fuse to the plasma membrane in NGF-treated PC12 cells. Therefore, activity of TC10 at vesicles is presumed to be inactivated near the plasma membrane during neuronal exocytosis. Our model is supported by functional evidence that constitutively active TC10 could not rescue decrease in NGF-induced neurite outgrowth induced by TC10 depletion. Furthermore, TC10 knockdown experiments and colocalization analyses confirmed the involvement of Exo70 in TC10-mediated trafficking in neuronal cells. TC10 frequently resided on vesicles containing Rab11, which is a key regulator of recycling pathways and implicated in neurite outgrowth. In growth cones, most of the vesicles containing the cell adhesion molecule L1 had TC10. Exocytosis of Rab11- and L1-positive vesicles may play a central role in TC10-mediated neurite outgrowth. The combination of this study and our previous work on the role of TC10 in EGF-induced exocytosis in HeLa cells suggests that the signaling machinery containing TC10 proposed here may be broadly used for exocytosis.
    Keywords Medicine ; R ; Science ; Q
    Subject code 571
    Language English
    Publishing date 2013-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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