Study on the reactivation of regenerative ability by masking 'autoantigens' expressed in organ blastema.

2016 Fiscal Year Final Research Report

• Project/Area Number: 26640051
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Laboratory animal science
• Research Institution: The University of Tokyo
• Principal Investigator: Kubo Takeo 東京大学, 大学院理学系研究科(理学部), 教授 (10201469)
• Research Collaborator: SHIRAHIGE Katsuhiko 東京大学, 分子細胞生物学研究所, 教授 (90273854) ; KATOU Yuki 東京大学, 分子細胞生物学研究所, 助教 (50391917)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: アフリカツメガエル / 器官再生 / 未分化増殖細胞 / インターロイキン-11 / ゲノム編集 / PhyH-like / Phyhd1 / T細胞活性化

Outline of Final Research Achievements

Xenopus laevis tadpoles transiently lose their tail regenerative ability during the ‘refractory period’, probably because immature leukocytes attack proliferating tail blastemal cells as ‘non-self’ during the period. In the present study, we aimed to clarify molecular mechanisms underlying tail regeneration through functional analyses of interleukin-11 (il-11), which is selectively expressed in the proliferating tail blastemal cells, and XPhyh-like, which is a putative marker gene for leukocytes that attack tail blastemal cells.
The results indicated that il-11 is necessary for tail regeneration and play important roles in the induction and maintenance of undifferentiated cells of various tissue origin in tail blastema. In addition, XPhyH-like was suggested to be related to impaired tail regenerative ability caused by immature leukocytes, because murine XPhyH-like homologue (Phyhd1) was induced in leukocytes accompanied with the leukocyte activation.

Free Research Field

動物生理化学