2022 Fiscal Year Final Research Report
Synaptic regulation by microglia through atypical cadherin Fat3
| Project/Area Number |
20K05951
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Review Section |
Basic Section 38060:Applied molecular and cellular biology-related
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| Research Institution | University of Tsukuba |
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Principal Investigator |
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| Project Period (FY) |
2020-04-01 – 2023-03-31
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| Keywords | FAT3 / ミクログリア / シナプス |
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| Outline of Final Research Achievements |
After birth, microglia extend their projections and change into complex morphologies. Recently, it has been suggested that during this process, microglia remove unnecessary synapses and construct precise neural circuits. However, the mechanism of synaptic pruning by microglia remains unclear. Previously, the applicant has searched for factors that induce morphological changes in microglia and identified an atypical cadherin family protein, Fat3. In this project, we analyzed Fat3 knockout mice and found that Fat3 accelerates postnatal microglial maturation and synaptic pruning. These results propose a new mechanism for synaptic regulation by microglia.
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| Free Research Field |
神経科学 分子生物学
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| Academic Significance and Societal Importance of the Research Achievements |
これまでミクログリアは、脳内の免疫担当細胞として、主に炎症応答や死細胞の除去などに関与することが示唆されていた。しかし近年、ミクログリアは、シナプスの形成や刈り込み、神経幹細胞の増殖分化、脳血管の機能制御など、多彩な機能を示すことが明らかとなりつつある。本研究課題は、これまでミクログリアの制御因子としての解析は行われてこなかった非定型カドヘリンファミリータンパク質Fat3に着目し、ミクログリア成熟との関連を示した点が学術的意義のある点だと考えている。
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