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Your search keyword '"Kamiguchi, Hiroyuki"' showing total 356 results
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356 results on '"Kamiguchi, Hiroyuki"'

16. Shootin1 interacts with actin retrograde flow and L1-CAM to promote axon outgrowth

Author

Shimada, Tadayuki, Toriyama, Michinori, Uemura, Kaori, Kamiguchi, Hiroyuki, Sugiura, Tadao, Watanabe, Naoki, Inagaki, Naoyuki, Shimada, Tadayuki, Toriyama, Michinori, Uemura, Kaori, Kamiguchi, Hiroyuki, Sugiura, Tadao, Watanabe, Naoki, and Inagaki, Naoyuki

Abstract

Actin polymerizes near the leading edge of nerve growth cones, and actin filaments show retrograde movement in filopodia and lamellipodia. Linkage between actin filament retrograde flow and cell adhesion molecules (CAMs) in growth cones is thought to be one of the mechanisms for axon outgrowth and guidance. However, the molecular basis for this linkage remains elusive. Here, we show that shootin1 interacts with both actin filament retrograde flow and L1-CAM in axonal growth cones of cultured rat hippocampal neurons, thereby mediating the linkage between them. Impairing this linkage, either by shootin1 RNA interference or disturbing the interaction between shootin1 and actin filament flow, inhibited L1-dependent axon outgrowth, whereas enhancing the linkage by shootin1 overexpression promoted neurite outgrowth. These results strengthen the actin flow-CAM linkage model (clutch model) for axon outgrowth and suggest that shootin1 is a key molecule involved in this mechanism.

Published
2023

37. Shootin1 interacts with actin retrograde flow and L1-CAM to promote axon outgrowth

Author

Shimada, Tadayuki, Toriyama, Michinori, Uemura, Kaori, Kamiguchi, Hiroyuki, Sugiura, Tadao, Watanabe, Naoki, and Inagaki, Naoyuki

Subjects
Muscle proteins -- Influence, Actin -- Influence, Cell adhesion molecules -- Properties, Axons -- Growth, Company growth, Biological sciences
Abstract

Actin polymerizes near the leading edge of nerve growth cones, and actin filaments show retrograde movement in filopodia and lamellipodia. Linkage between actin filament retrograde flow and cell adhesion molecules (CAMs) in growth cones is thought to be one of the mechanisms for axon outgrowth and guidance. However, the molecular basis for this linkage remains elusive. Here, we show that shootin1 interacts with both actin filament retrograde flow and L1-CAM in axonal growth cones of cultured rat hippocampal neurons, thereby mediating the linkage between them. Impairing this linkage, either by shootin1 RNA interference or disturbing the interaction between shootin1 and actin filament flow, inhibited L1-dependent axon outgrowth, whereas enhancing the linkage by shootin1 overexpression promoted neurite outgrowth. These results strengthen the actin flow-CAM linkage model ('clutch' model) for axon outgrowth and suggest that shootin1 is a key molecule involved in this mechanism.

Published
2008

42. Cell adhesion molecules regulate [Ca.sup.2+]-mediated steering of growth cones via cyclic AMP and ryanodine receptor type 3

Author

Ooashi, Noriko, Futatsugi, Akira, Yoshihara, Fumie, Mikoshiba, Katsuhiko, and Kamiguchi, Hiroyuki

Subjects
Cell adhesion molecules -- Research, Nervous system -- Degeneration, Nervous system -- Research, Biological sciences
Abstract

Axonal growth cones migrate along the correct paths during development, not only directed by guidance cues but also contacted by local environment via cell adhesion molecules (CAMs). Asymmetric [Ca.sup.2+] elevations in the growth cone cytosol induce both attractive and repulsive turning in response to the guidance cues (Zheng, J.Q. 2000. Nature. 403:89-93; Henley, J.R., K.H. Huang, D. Wang, and M.M. Poo. 2004. Neuron. 44:909-916). Here, we show that CAMs regulate the activity of ryanodine receptor type 3 (RyR3) via cAMP and protein kinase A in dorsal root ganglion neurons. The activated RyR3 mediates [Ca.sup.2+]-induced [Ca.sup.2+] release (CICR) into the cytosol, leading to attractive turning of the growth cone. In contrast, the growth cone exhibits repulsion when [Ca.sup.2+] signals are not accompanied by RyR3-mediated CICR. We also propose that the source of [Ca.sup.2+] influx, rather than its amplitude or the baseline [Ca.sup.2-] level, is the primary determinant of the turning direction. In this way, axon-guiding and CAM-derived signals are integrated by RyR3, which serves as a key regulator of growth cone navigation.

Published
2005

45. L1-dependent neuritogenesis involves [ankyrin.sub.B] that mediates L1-CAM coupling with retrograde actin flow

Author

Nishimura, Kazunari, Yoshihara, Fumie, Tojima, Takuro, Ooashi, Noriko, Yoon, Woohyun, Mikoshiba, Katsuhiko, Bennett, Vann, and Kamiguchi, Hiroyuki

Subjects
Cells -- Research, Molecules -- Research, Biological sciences
Abstract

The cell adhesion molecule L1 (L1-CAM) plays critical roles in neurite growth. Its cytoplasmic domain (L1CD) binds to ankyrins that associate with the spectrin-actin network. This paper demonstrates that L1-CAM interactions with [ankyrin.sub.B] (but not with [ankyrin.sub.G]) are involved in the initial formation of neurites. In the membranous protrusions surrounding the soma before neuritogenesis, filamentous actin (F-actin) and [ankyrin.sub.G] continuously move toward the soma (retrograde flow). Bead-tracking experiments show that [ankyrin.sub.B] mediates L1-CAM coupling with retrograde F-actin flow in these perisomatic structures. Ligation of the L1-CAM ectodomain by an immobile substrate induces L1CD-[ankyrin.sub.B] binding and the formation of stationary [ankyrin.sub.B] clusters. Neurite initiation preferentially occurs at the site of these clusters. In contrast, [ankyrin.sub.B] is involved neither in L1-CAM coupling with F-actin flow in growth cones nor in L1-based neurite elongation. Our results indicate that [ankyrin.sub.B] promotes neurite initiation by acting as a component of the clutch module that transmits traction force generated by F-actin flow to the extracellular substrate via L1-CAM.

Published
2003

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