Tara Yuki

写真a

Title

Assistant Professor

Current Affiliation Organization 【 display / non-display 】

  • Duty   University of the Ryukyus   Graduate School of Medicine   Assistant Professor  

University 【 display / non-display 】

  •  
    -
    2025.08

    Okinawa Institute of Science and Technology Graduate University     Graduated

Academic degree 【 display / non-display 】

  •  -  Ph.D.

External Career 【 display / non-display 】

  • 2024.04
    -
    2025.08

    Okinawa Institute of Science and Technology Graduate University  

  • 2025.09
    -
    2026.03

    Okinawa Institute of Science and Technology Graduate University  

  • 2026.04
     
     

    University of the Ryukyus  

Research Interests 【 display / non-display 】

  • 遺伝子発現制御

  • 膵β細胞

  • 糖尿病

  • RNA代謝

  • mRNA分解

Research Areas 【 display / non-display 】

  • Life Science / Pathological biochemistry

  • Life Science / Molecular biology

  • Life Science / Metabolism and endocrinology

Published Papers 【 display / non-display 】

  • Post-transcriptional regulation by the CCR4-NOT deadenylase complex maintains redox homeostasis in insulin biosynthesis in mouse pancreatic β cells

    Akiko Yanagiya, Patrick N. Stoney, Yuki Tara, Shohei Takaoka, Guillaume Vares, Rei Higa, Nicholas R. Friedman, Alejandro Villar-Briones, Tadashi Yamamoto

    ( openRxiv )    2024.06

    Type of publication: Research paper (other science council materials etc.)

     View Summary

    SUMMARY Pancreatic β cells synthesize insulin to maintain glucose homeostasis. In diabetes, elevated blood glucose and insulin resistance compel β cells to produce insulin, and hence β cells are vulnerable to oxidative stress by glucotoxicity. In insulin biosynthesis, the conversion of proinsulin to insulin is initiated by forming disulfide bonds in proinsulin for oxidative protein folding. Insulin content and insulin secretion in β cells are decreased by deletion of CNOT7, a catalytic subunit of the CCR4-NOT complex, and accompanied by increased proinsulin, implying the impaired conversion of proinsulin to insulin. We found that PRDX4 essential for disulfide bond formation in proinsulin, is reduced in Cnot7 -KO β cells. Moreover, protein expression of CNOT8, a paralog of CNOT7, is increased in Cnot7 -KO β cells and binds to Prdx4 mRNA via MSI2. Here, we demonstrate the post-transcriptional regulation of Prdx4 mRNA by the CCR4-NOT complex to maintain oxidative-reductive homeostasis in insulin biosynthesis. HIGHLIGHTS Insulin content and secretion are decreased in Cnot7 -KO pancreatic β cells. PRDX4, needed for proinsulin folding, is decreased in Cnot7 -KO pancreatic islets. The conversion of proinsulin to insulin is impaired in Cnot7 -KO β cells. CNOT8, but not CNOT7, interacts with MSI2 that binds to Prdx4 mRNA

  • The multi-level regulation of clownfish metamorphosis by thyroid hormones.

    Natacha Roux, Saori Miura, Mélanie Dussenne, Yuki Tara, Shu-Hua Lee, Simon de Bernard, Mathieu Reynaud, Pauline Salis, Agneesh Barua, Abdelhay Boulahtouf, Patrick Balaguer, Karine Gauthier, David Lecchini, Yann Gibert, Laurence Besseau, Vincent Laudet

    Cell reports   42 ( 7 ) 112661 - 112661   2023.07 [ Peer Review Accepted ]

    Type of publication: Research paper (scientific journal)

     View Summary

    Most marine organisms have a biphasic life cycle during which pelagic larvae transform into radically different juveniles. In vertebrates, the role of thyroid hormones (THs) in triggering this transition is well known, but how the morphological and physiological changes are integrated in a coherent way with the ecological transition remains poorly explored. To gain insight into this question, we performed an integrated analysis of metamorphosis of a marine teleost, the false clownfish (Amphiprion ocellaris). We show how THs coordinate a change in color vision as well as a major metabolic shift in energy production, highlighting how it orchestrates this transformation. By manipulating the activity of liver X regulator (LXR), a major regulator of metabolism, we also identify a tight link between metabolic changes and metamorphosis progression. Strikingly, we observed that these regulations are at play in the wild, explaining how hormones coordinate energy needs with available resources during the life cycle.

  • Nobiletin ameliorates glucose tolerance by protecting against β-cell loss in type-2 diabetic db/db mice

    Yukiko K. Kaneko, Yuki Tara, Stella Amarachi Ihim, Moe Yamamoto, Megumi Kaji, Tomohisa Ishikawa

    Phytomedicine Plus ( Elsevier BV )  2 ( 4 ) 100367 - 100367   2022.11 [ Peer Review Accepted ]

    Type of publication: Research paper (scientific journal)

Presentations 【 display / non-display 】

  • Turnover of mRNA mediated by RNA modification regulates pancreatic β cell function and identity

    Yuki Tara, Tadashi Yamamoto

    60th European Association for the Study of Diabetes (EASD) Annual Meeting  (Madrid, Spain)  1900.01  -  1900.01 

Academic Awards 【 display / non-display 】

  • Competitive Travel Grant (EASD 2024)

    2024.09   European Association for the Study of Diabetes (EASD)  

Grant-in-Aid for Scientific Research 【 display / non-display 】

  • Pathophysiology of diabetes mediated by mRNA turnover in pancreatic beta cells

    Grant-in-Aid for JSPS Fellows

    Project Year: 2024.04  -  2026.03 

    Direct: 1,600,000 (YEN)  Overheads: 1,600,000 (YEN)  Total: 0 (YEN)