Long term maintenance of pluripotenst stem cells by GAP junction in planarian

2022 Fiscal Year Final Research Report

• Project/Area Number: 20K06677
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 44020:Developmental biology-related
• Research Institution: Tsuyama National College of Technology
• Principal Investigator: SHIBATA Norito 津山工業高等専門学校, 総合理工学科, 教授 (60402781)
• Project Period (FY): 2020-04-01 – 2023-03-31
• Keywords: 全能性幹細胞 / MTA / 再生 / プラナリア

Outline of Final Research Achievements

Although planarians maintain pluripotent stem cells named neoblasts widely distributed throughout mesenchymal space, the molecular mechanism for the neoblast maintenance is still unknown. In this study, I aimed to reveal the mechanism for the neoblast maintenance. Dysfunction of planarian MTA homolog genes, MTA-A and MTA-B, by RNAi caused alternation of distribution pattern of neoblasts and regenerative defect simultaneously. This suggest that distribution pattern seemed in MTA knockdown planarians might be involved in maintenance of neoblasts. Double knockdown of MTA-A and a planarian innexin gene, inx-B, that is used in GAP junction could rescue the phenotype observed in MTA-A single knockdown planarians. In contrast to this, simultaneous knockdown of MTA-B and inx-B could not affect phenotype of MTA-B single knockdown planarians, suggesting that there are two mechanisms for neoblast maintenance using different MTA genes in planarians.

Free Research Field

発生生物学

Academic Significance and Societal Importance of the Research Achievements

ヒトでは不可能な、生体内で長期にわたって分化全能性幹細胞を維持しているプラナリアから、その機構を学ぶことを本研究の目的とした。その結果、プラナリアはMTA遺伝子の発現を制御することで、幹細胞の接着性を変化させ、その結果、幹細胞の維持を行っている可能性を示唆できた。
in vitroにおいても長期間の維持の困難な全能性幹細胞を、良い状態で維持できる内在的な仕組みの一端を示すことができた本研究は、基礎的な再生研究に対して学術的な意義があり、さらに今後の再生医療の発展に寄与できる社会的意義を持つ。