Tracheal motile cilia in mice require CAMSAP3 for the formation of central microtubule pair and coordinated beating

Author:

Saito Hiroko1,Matsukawa-Usami Fumiko2,Fujimori Toshihiko2,Kimura Toshiya1,Ide Takahiro3,Yamamoto Takaki4,Shibata Tatsuo5,Onoue Kenta6,Okayama Satoko6,Yonemura Shigenobu6,Misaki Kazuyo7,Soba Yurina8,Kakui Yasutaka89,Sato Masamitsu8,Toya Mika1810,Takeichi Masatoshi1

Affiliation:

1. Laboratory for Cell Adhesion and Tissue Patterning

2. Division of Embryology, National Institute for Basic Biology, and Department of Basic Biology, School of Life Science, SOKENDAI, the Graduate University for Advanced Studies, Okazaki, 444-8787 Japan

3. Laboratory for Organismal Patterning

4. Nonequilibrium Physics of Living Matter RIKEN Hakubi Research Team

5. Laboratory for Physical Biology, and

6. Ultrastructural Research Team, RIKEN Center for Life Science Technologies, Kobe 650-0047, Japan

7. Laboratory for Ultrastructural Research, RIKEN Center for Biosystems Dynamics Research, Kobe 650-0047, Japan

8. Laboratory of Cytoskeletal Logistics, Center for Advanced Biomedical Sciences (TWIns), Waseda University, Tokyo 162-8480, Japan

9. Waseda Institute for Advanced Study, Waseda University, Tokyo 169-0051, Japan

10. Major in Bioscience, Global Center for Science and Engineering, Faculty of Science and Engineering, Waseda University, Tokyo 169-8555, Japan

Abstract

CAMSAP3, a protein that controls microtubule dynamics by binding to its minus-end, is localized at proximal regions of the axoneme in tracheal motile cilia. Its dysfunction results in a collapse of the central microtube pair, basal plate disorganization, and uncoordinated beating of multicilia.

Publisher

American Society for Cell Biology (ASCB)

Subject

Cell Biology,Molecular Biology

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