Mechanical and pathological analyses of shootin-mediated brain formation

2016 Fiscal Year Final Research Report

• Project/Area Number: 26290007
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Neurophysiology / General neuroscience
• Research Institution: Nara Institute of Science and Technology
• Principal Investigator: Naoyuki Inagaki 奈良先端科学技術大学院大学, バイオサイエンス研究科, 教授 (20223216)
• Co-Investigator(Renkei-kenkyūsha): URASAKI Akihiro 奈良先端科学技術大学院大学, バイオサイエンス研究科, 助教 (40550083) ; SAKUMURA Yuichi 愛知県立大学, 情報科学研究科, 准教授 (40550083)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: Shootin / 大脳組織形成 / ノックアウトマウス / ゼブラフィッシュ / メカノバイオロジー

Outline of Final Research Achievements

Force interaction between cells and adhesive substreates induces cell migration that plays a key role in tissue morphogenesis. However, the molecular mechanics how cells generate forces between cells and substreates for cell migration and tissue morphogenesis remains unclear. Shootin1 is a brain-specific protein involved in axon formation. We found a novel splicing isoform of shootin1 which is expressed not only in the brain but also in peripheral tissues. We renamed the brain-specific shootin1 as shootin1a and termed the novel isoform as shootin1b. We found that shootin1 is involved in migration of olfactory neurons and formation of the olfactory bulb. Shootin1b interacts with actin filaments that undergo directional polymerization at the leading edge of migrating olfactory neurons. Our data suggest shootin1b mediates the linkage between the actin filaments and the cell adhesion molecule L1-CAM, thereby generating forces between cell’s leading and and substreates for migration.

Free Research Field

細胞生物学、神経科学、メカノバイオロジー、システム生物学