敵対的な遺伝子パラログであるUpf3aとUpf3bは,無意味な媒介によるRNA分解を制御する
Eleen Y Shum1, Samantha H Jones1, Ada Shao1
1Department of Reproductive Medicine, School of Medicine, University of California San Diego, La Jolla, CA 92103, USA.
Cell
|April 5, 2016
まとめ
遺伝子の複製により UPF3Aが生まれました これはNMD阻害剤で トランスクリプトを安定させます UPF3Aの喪失はハイパーNMDを引き起こし,マウスの発達障害を引き起こします.
科学分野:
- 進化生物学
- 分子遺伝学
- 発達生物学
背景:
- 遺伝子の複製は進化を促し 新しい機能を生み出します
- UPF3B遺伝子は,ナンセンス媒介RNA分解 (NMD) に不可欠である.
- その複製体UPF3Aは,NMDの活性が最小限で,機能が不明である.
研究 の 目的:
- UPF3Aの機能を調べる
- 対抗性遺伝子の機能の進化的メカニズムを決定する.
- 開発におけるUPF3Aの役割を理解する.
主な方法:
- インビトロとインビボの機能喪失実験
- トランスクリプトの安定性の分析
- UPF3A機能を研究する条件付きノックアウトマウスモデル.
- 胚形成と胚形成の欠陥の評価
主要な成果:
- UPF3Aは,ナンセンス媒介RNA分解 (NMD) の強力な阻害剤として機能する.
- UPF3Aは,NMDを抑制することで何百ものトランスクリプトを安定させます.
- UPF3Aの抑制活性に 障害のあるドメイン獲得が 根底にある可能性が高い.
- UPF3Aが欠けているマウスは NMDと発達障害を呈する.
結論:
- UPF3Aは,発達の過程でNMDを調節する分子リオスタットとして作用する.
- 遺伝子の複製から生じる敵対的な機能は急速な進化的メカニズムである.
- NMDにおけるUPF3Aの役割は,正常な胚形成とゲメト形成に不可欠です.
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