Actomyosin-based control of tissue morphology

2020 Fiscal Year Final Research Report

• Project/Area Number: 17K17799
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Morphology/Structure; Cell biology
• Research Institution: Kumamoto University (2020); Nagoya University (2017-2019)
• Principal Investigator: Shindo Asako 熊本大学, 発生医学研究所, 准教授 (60512118)
• Project Period (FY): 2017-04-01 – 2021-03-31
• Keywords: アクトミオシン / 創傷修復 / 細胞運動 / 組織形態 / アフリカツメガエル / 胚

Outline of Final Research Achievements

Actomyosin is one of the conserved driving forces of tissue morphogenesis during animal development, and its regulatory molecules are significant to understand the processes of morphogenesis. In this study, we used Xenopus laevis embryo as a model system and found that the cytoskeletal interactions assist actomyosin contractility in facilitating wound closure in the developing epidermis (Shindo et al., 2018). To identify the regulatory molecules of actomyosin contractility, we established chemical screening using Xenopus embryos. By investigating one of the candidate molecules we detected from the screening, we found the molecular mechanism required for balancing the actomyosin contractility to maintain normal cell shape in the epidermis. Our findings illuminate molecular mechanisms for fine-tuning of actomyosin contractility both in dynamic and stable cell behaviors during morphogenesis.

Free Research Field

発生生物学

Academic Significance and Societal Importance of the Research Achievements

正常な胚発生過程で細胞の形態変化や移動を駆動することが知られていたアクトミオシンの機能を、胚表皮の創傷修復過程といういわば「異常状態」を解析したことにより、アクトミオシンが多様な組織や現象に適応し利用されるメカニズムの一端を明らかにした。胚表皮の創傷修復を制御する分子を探索したことにより、なぜ胚は成体と異なり創傷を早く治すことができるのかという根源的な疑問に答えるためのヒントが得られ、胚の創傷修復研究を推進した。