Mechanism of CCR4-NOT complex-mediated target mRNA degradation in B cells

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K19127
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Immunology
• Research Institution: Osaka University
• Principal Investigator: Inoue Takeshi 大阪大学, 免疫学フロンティア研究センター, 特任助教(常勤) (80466838)
• Project Period (FY): 2015-04-01 – 2017-03-31
• Keywords: B細胞分化 / CCR4-NOT複合体 / mRNA分解 / 免疫グロブリン遺伝子再構成

Outline of Final Research Achievements

The CCR4-NOT deadenylase complex plays crucial roles in mRNA decay and translational repression induced by poly(A) tail shortening. We have previously found a severe impairment of early B cell development in mice lacking CNOT3 subunit of this complex. Here, we analyzed the underlying molecular mechanisms, and our data suggested that the CCR4-NOT complex regulates B cell differentiation by controlling Igh rearrangement and destabilizing p53 mRNA.

Free Research Field

免疫学、分子生物学