Study of resistance capacitation mechanism against actin polymerization inhibitors in Tetrahymena

2014 Fiscal Year Final Research Report

• Project/Area Number: 24657128
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Cell biology
• Research Institution: University of Tsukuba
• Principal Investigator: NUMATA Osamu 筑波大学, 生命環境系, 教授 (50189354)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: テトラヒメナ / アクチン / ラトランキュリンA / 薬剤耐性 / 細胞質分裂 / 食胞形成 / 遺伝子過剰発現株 / ゾウリムシ

Outline of Final Research Achievements

For the solution to the molecular mechanism of "specific drug resistance capacitation against actin polymerization inhibitors in Tetrahymena thermophila", we focused on the actin gene Act2. Its expression amount was increased by actin polymerization inhibitor Lat-A. We destroyed the Act2 gene. In Act2 gene disrupted strain, it could not acquire the drug-resistant ability. Thus, by expression of the Act2, it concludes that specific drug resistance ability against actin polymerization inhibitors is acquired. In addition, in nutrition growth phase, a treatment of Lat-A to Act2 gene KO strain inhibited progression from a G2 phase to a mitotic phase. In starvation, the treatment of Lat-A to Act2 gene KO strain inhibited autophagy. Moreover, because there was actin polymerization inhibitor resistance ability in Paramecium tetraurelia, it suggests that this nature is common in ciliates.

Free Research Field

細胞生物学