トリム28 ハプロイン不足がバイ安定性表遺伝子肥満を誘発する
Kevin Dalgaard1, Kathrin Landgraf2, Steffen Heyne1
1Max Planck Institute of Immunobiology and Epigenetics, Stübeweg 51, 79108 Freiburg, Germany.
Cell
|January 30, 2016
まとめ
研究者らは Trim28に依存する遺伝子ネットワークを発見し "オン/オフ"の方法で肥満を誘発することができました この発見は 肥満の遺伝性の新しいメカニズムを明らかにし 複雑な特性を理解するための意味合いがあります
科学分野:
- 遺伝学
- 発達生物学
- 代謝障害
背景:
- 肥満は世界中で50億人以上の人々に 影響を及ぼしており 伝統的なメンデルの遺伝学では説明できない 重要な遺伝性があります
- 肥満の遺伝的基盤を理解することは 効果的な治療法の開発に不可欠です
研究 の 目的:
- 肥満の遺伝性に関与する新しい遺伝子ネットワークを特定する.
- 体重と遺伝子発現の調節におけるTrim28の役割を調査する.
- マウスとヒトの両方の肥満におけるポリフェニズムの可能性を調査する.
主な方法:
- Trim28(+/D9) 変異マウスを用いて体重分布と遺伝子発現を研究した.
- 肥満と正常なマウスのインプリント遺伝子ネットワーク (Nnat,Peg3,Cdkn1c,Plagl1) の発現を分析した.
- 脂肪組織のトランスクリプトーム解析を人間の子供で行いました.
主要な成果:
- トリム28 ((+/D9) の突然変異のマウスは,体重のバイモダル分布を示し,ストキャスティックな肥満の現象型を示した.
- 肥満状態は 特定のインプリントされた遺伝子の発現の減少と相関しています
- 人間の子供は Trim28の発現とインプリントされた遺伝子不調に基づいて,マウスの表型を反映した異なるサブ集団を示した.
結論:
- トリム28に依存するネットワークを特定し 肥満を誘発する メンデルのような "オン/オフ"のやり方ではありません
- マウスとヒトの両方の肥満における離散型ポリフェニズムに関する証拠を提供した.
- 複雑な特性の遺伝学,進化,医学への影響を強調した.
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