Mechanism of cell death suppression by Ptch1 and XIAP during mouse embryogenesis

2020 Fiscal Year Final Research Report

• Project/Area Number: 17K08513
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: General anatomy (including histology/embryology)
• Research Institution: Hamamatsu University School of Medicine
• Principal Investigator: aoto kazushi 浜松医科大学, 医学部, 助教 (60360476)
• Project Period (FY): 2017-04-01 – 2021-03-31
• Keywords: ソニックヘッジホッグ(Shh)シグナル伝達経路 / patched1 / 脳神経管の細胞死抑制 / CRISPR-Cas9法 / GONAD法 / XIAP / エレクトロポレーション / 繊毛

Outline of Final Research Achievements

To analyze physiological function of inhibiting cell death oy Ptch1-XIAP association, we generated mutant mice of XIAP binding site with Ptch1 C terminus. But that Ptch1-dIBS mice did not show any phenotype. However, We also generated knock-in mice of two HA tag (2xHA) in Ptch1 C terminal, which are able to observe Ptch1-2xHA localization in cilia.

Free Research Field

発生学

Academic Significance and Societal Importance of the Research Achievements

ヘッジホッグシグナルの受容体Ptch1は、奇形と高発癌性の基底細胞母斑症候群（ゴーリン症候群）の原因遺伝子である。本研究は、奇形発症の機序を理解する助けとなるだけでなく、Ptch1機能欠失による発癌の抑制を行える可能性を示した。