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2019 Fiscal Year Final Research Report

Molecular mechanism of emotional dysfunction in mouse model of neurodevelopmental disorders: focusing on alternative polyadenylation

Research Project

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Project/Area Number 17K10081
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Pediatrics
Research InstitutionGifu Pharmaceutical University

Principal Investigator

Fukumitsu Hidefumi  岐阜薬科大学, 薬学部, 教授 (00308280)

Co-Investigator(Kenkyū-buntansha) 宗宮 仁美  岐阜薬科大学, 薬学部, 助教 (20548713)
Project Period (FY) 2017-04-01 – 2020-03-31
Keywords神経発達障害 / 選択的 polyA 付加反応
Outline of Final Research Achievements

Xa gene deficient mice, one of the key regulators of alternative polyadenylation (APA), showed social behavioral abnormalities with stress-sensitive neural circuits. Subsequent in vitro analyses revealed that Xa affects the various cellular properties in a dose-dependent manner, especially against cell mobilities. Xa was also found to influence on transcriptome by regulating with the length of target gene mRNA’s 3'UTR than the expression levels. These alterations in the neural circuits and in the molecular bases are believed to be linked to behavioral abnormalities in Xa gene-modified mice.

Free Research Field

神経科学

Academic Significance and Societal Importance of the Research Achievements

知的障害や自閉症スペクトラム障害を含む神経発達障害の患者数は近年増加傾向にあるが、発症機序は不明なところが多い。一般に、多くの遺伝子 mRNA 前駆体は複数のpolyA付加部位をもち、その選択により3′UTR長の異なる多様な mRNA を生成する(選択的 polyA 付加反応: APA)。病態との関係は不明であるが、近年、神経発達障害の患者脳で APA の制御不全の可能性を示唆するデータが集積しつつある。本研究では、遺伝子改変マウスを用いて、APA の主要な制御因子である Xa の欠損が情動制御や社会性行動異常と関連することを明らかにし、分子機構の一部を明らかにした。

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Published: 2021-02-19  

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