Molecular mechanisms of collective cell movement during wound healing

2014 Fiscal Year Final Research Report

• Project/Area Number: 26891012
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Single-year Grants
• Research Field: Cell biology
• Research Institution: Nagoya University
• Principal Investigator: SHINDO Asako 名古屋大学, 理学(系)研究科(研究院), 助教 (60512118)
• Project Period (FY): 2014-08-29 – 2015-03-31
• Keywords: 創傷治癒 / 細胞集団 / 細胞骨格

Outline of Final Research Achievements

Collective cell movement is a fundamental cellular event for tissue morphogenesis and repair. The molecular mechanisms of the coordinated cell behaviors are largely unknown. In this research, we have focus on embryonic epithelial wound healing as a model, and　analyzed the process of cell shape change and cell movement. It has been known that the driving force for cell movement during embryonic wound closure is contractile force generated by actomyosin at the wound edge. We have found that the actomyosin requires septins, a cytoskeletal element, to close the wound. We concluded that septins controls cell shape and movement to coordinate the collective cell movement in the tissue via actomyosin.

Free Research Field

細胞生物学、発生生物学