Elucidation of mechanisms related to actin cytoskeleton dynamics of dedifferentiation and acquisition of multipotency in mature adipocytes

2018 Fiscal Year Final Research Report

• Project/Area Number: 16K18822
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Integrative animal science
• Research Institution: Nihon University
• Principal Investigator: OKI Yoshinao 日本大学, 生物資源科学部, 助教 (70525667)
• Project Period (FY): 2016-04-01 – 2019-03-31
• Keywords: 脂肪細胞 / アクチン細胞骨格 / 脱分化

Outline of Final Research Achievements

During the mature adipocyte dedifferentiation, loss of lipid droplets occurs with remodeling of actin cytoskeleton. Transcriptome analysis identified MKL1 also known as actin-binding transcriptional coactivator, as upregulated gene after dedifferentiation of mature adipocyte. Formation of actin stress fiber in dedifferentiation of mature adipocyte resulted in the nuclear accumulation of MKL1. Furthermore, the formation of actin stress fibres and the nuclear translocation of MKL1 was accompanied by a marked decrease in the expression of PPARγ. These results suggest that regulation of MKL1 by actin cytoskeleton dynamics is a critical part of dedifferentiation of mature adipocytes.

Free Research Field

細胞生物学

Academic Significance and Societal Importance of the Research Achievements

本研究は極めて簡便な方法によって体細胞から脱分化および多能性獲得した細胞を大量に取得できる独自の培養系を用いて、その仕組みを解明するものである。幹細胞のみが具備すると考えられている多能性について、脱分化細胞がなぜその能力を有するのかを明らかにすることは、一個の受精卵から多種多様な機能をもつ細胞（分化細胞）が生ずる仕組みの解明に大きく貢献すると考えられる。