SIRT6欠乏はシノモルグスの猿の発達遅延を引き起こす

Weiqi Zhang^1,2,3,4, Haifeng Wan^2,3,4, Guihai Feng^2,3,4

¹National Laboratory of Biomacromolecules, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.

Nature

|August 24, 2018

まとめ

SIRT6は霊長類の発達に不可欠です猿のSIRT6の喪失は,H19の活性化によって神経の分化が妨げられ,人間の発達障害への洞察をもたらします.

科学分野:

遺伝学と発達生物学
霊長類のモデル
エピジェネティクス

背景:

SIRT6は,歯類における長寿タンパク質として認識されています.
霊長類の発達におけるSIRT6の特定の役割は,ほとんど特徴づけられていない.
類人猿のSIRT6の機能を理解することは,比較生物学と人間の健康にとって不可欠です.

研究の目的:

靈長類におけるSIRT6の生物学的機能を調査する.
SIRT6ゼロのシノモルグス猿のモデルを作り,特徴づけること.
発達におけるSIRT6の役割の基礎となる分子メカニズムを解明する.

主な方法:

CRISPR-Cas9 遺伝子編集により SIRT6 ゼロのシノモルグス猿が生まれました
SIRT6欠乏したサルにおける胎児の発達と生存率の分析
ニューロンの分化とH19の調節を検証するために,ヒトの神経原始細胞を用いたインビトロ研究.

主要な成果:

SIRT6欠乏したサルは,重度の産前発達遅延を示し,出生直後に死亡します.
SIRT6の喪失は,長い非コーディングRNAH19の転写活性化により遅れた神経分化につながります.
SIRT6欠乏は,H19インプリント制御領域でヒストンの過酸化を引き起こし,H19の発現を増加させます.

結論:

SIRT6は,ヒト以外の霊長類の産前発達を調節する上で重要な役割を果たします.
このメカニズムは,SIRT6が重要な発達抑制体であるH19の調節を伴う.
これらの発見は,ヒトの生後死亡症候群に関する潜在的メカニズム的な洞察を提供します.

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