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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Abe, Takashi Yamazaki, Daisuke Murakami, Satoshi Hiroi, Makoto Nitta, Yohei Maeyama, Yuko Tabata, Tetsuya |
| Description | Country affiliation: Japan Author Affiliation: Abe T ( Institute of Molecular and Cellular Biosciences, University of Tokyo, Tokyo 113-0032, Japan Graduate Program in Biophysics and Biochemistry, Graduate School of Science, University of Tokyo, Tokyo 113-0033, Japan.); Yamazaki D ( Institute of Molecular and Cellular Biosciences, University of Tokyo, Tokyo 113-0032, Japan.); Murakami S ( Institute of Molecular and Cellular Biosciences, University of Tokyo, Tokyo 113-0032, Japan.); Hiroi M ( Institute of Molecular and Cellular Biosciences, University of Tokyo, Tokyo 113-0032, Japan.); Nitta Y ( Institute of Molecular and Cellular Biosciences, University of Tokyo, Tokyo 113-0032, Japan.); Maeyama Y ( Institute of Molecular and Cellular Biosciences, University of Tokyo, Tokyo 113-0032, Japan.); Tabata T ( Institute of Molecular and Cellular Biosciences, University of Tokyo, Tokyo 113-0032, Japan Graduate Program in Biophysics and Biochemistry, Graduate School of Science, University of Tokyo, Tokyo 113-0033, Japan ttabata@iam.u-tokyo.ac.jp.) |
| Abstract | The Rac-Cofilin pathway is essential for cytoskeletal remodeling to control axonal development. Rac signals through the canonical Rac-Pak-LIMK pathway to suppress Cofilin-dependent axonal growth and through a Pak-independent non-canonical pathway to promote outgrowth. Whether this non-canonical pathway converges to promote Cofilin-dependent F-actin reorganization in axonal growth remains elusive. We demonstrate that Sickie, a homolog of the human microtubule-associated protein neuron navigator 2, cell-autonomously regulates axonal growth of Drosophila mushroom body (MB) neurons via the non-canonical pathway. Sickie was prominently expressed in the newborn F-actin-rich axons of MB neurons. A sickie mutant exhibited axonal growth defects, and its phenotypes were rescued by exogenous expression of Sickie. We observed phenotypic similarities and genetic interactions among sickie and Rac-Cofilin signaling components. Using the MARCM technique, distinct F-actin and phospho-Cofilin patterns were detected in developing axons mutant for sickie and Rac-Cofilin signaling regulators. The upregulation of Cofilin function alleviated the axonal defect of the sickie mutant. Epistasis analyses revealed that Sickie suppresses the LIMK overexpression phenotype and is required for Pak-independent Rac1 and Slingshot phosphatase to counteract LIMK. We propose that Sickie regulates F-actin-mediated axonal growth via the non-canonical Rac-Cofilin pathway in a Slingshot-dependent manner. |
| File Format | HTM / HTML |
| ISSN | 09501991 |
| e-ISSN | 14779129 |
| Journal | Development |
| Issue Number | 24 |
| Volume Number | 141 |
| Language | English |
| Publisher | The Company of Biologists |
| Publisher Date | 2014-12-01 |
| Publisher Place | Great Britain (UK) |
| Access Restriction | Open |
| Subject Keyword | Discipline Developmental Discipline Biology Actin Depolymerizing Factors Metabolism Actins Axons Physiology Drosophila Proteins Drosophila Growth & Development Mushroom Bodies Cytology Nerve Tissue Proteins Signal Transduction Rac1 Gtp-binding Protein Animals Genetics Immunohistochemistry Lim Kinases Phosphoprotein Phosphatases Research Support, Non-u.s. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Developmental Biology Molecular Biology |
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