Identification of cell competition mediators that maintain barrier function of epidermis

2018 Fiscal Year Final Research Report

• Project Area: Cell competition: a mechanism for survival of the fittest in the multi-cellular community
• Project/Area Number: 26114003
• Research Category: Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)
• Allocation Type: Single-year Grants
• Review Section: Biological Sciences
• Research Institution: Tohoku University (2016-2018); Institute of Physical and Chemical Research (2014-2015)
• Principal Investigator: Kuranaga Erina 東北大学, 生命科学研究科, 教授 (90376591)
• Research Collaborator: Umetsu Daiki ; Uechi Hiroyuki
• Project Period (FY): 2014-07-10 – 2019-03-31
• Keywords: 上皮組織 / バリア機能 / 恒常性維持 / 細胞死

Outline of Final Research Achievements

In this study, we considered the process of epithelial cell remodeling in Drosophila during metamorphosis as an example of physiological cell competition, and searched for factors that induce non-autonomous cell death by using genetic screening. Pvf1, a Drosophila homolog of vascular endothelial growth factor, was identified as a factor on the winner cell side. As a loser-side factor, myosin VI involved in vesicle transport endocytosis was identified. In addition, we also analyzed cell competition-like phenomena in other epithelial cell populations. We established an experimental material that enables analysis of cell competition in epithelial rearrangement and published it.

Free Research Field

細胞生物学、発生生物学

Academic Significance and Societal Importance of the Research Achievements

これまでの細胞競合研究には人工的な遺伝子操作が必須であり、その作製した細胞競合モデルを安定的に解析することによって、制御メカニズムの解明が効率的に行われてきた実績がある。一方で、生理的環境下における細胞競合が関与する生命現象およびその生理的意義に関する研究は未だ稀少である。本研究では、細胞競合の生理的環境下における細胞競合の制御メカニズムを探索し、進化的保存性の高い成長因子と小胞輸送に関与する分子を発見した。本研究で同定された分子が、前がん細胞の排除や上皮細胞の恒常性維持に重要であることが示唆されるため、今後の詳細なメカニズムの解明が期待される。