バクテリア感染におけるSIRT2依存ヒストンH3K18脱酸化の役割
Haig A Eskandarian1, Francis Impens, Marie-Anne Nahori
1Unité des Interactions Bactéries-Cellules, Institut Pasteur, Paris, France.
Science (New York, N.Y.)
|August 3, 2013
まとめ
病原性細菌は,デセチラゼシルトゥイン2 (SIRT2) をハイジャックすることで宿主細胞を再プログラムする. このエピジェネティックメカニズムは,SIRT2媒介ヒストンの脱エチル化を含み,細菌感染の成功に不可欠です.
科学分野:
- 微生物学 微生物学とは
- エピジェネティクス エピジェネティクス
- 分子生物学は分子生物学である.
背景:
- 病原体は,感染中に宿主細胞の転写を操作する.
- 病原体誘発の転写変化の背後にあるメカニズムは,しばしば不明である.
研究 の 目的:
- Listeria monocytogenes感染における宿主デセチラゼシルトゥイン2 (SIRT2) の役割を明らかにする.
- 病原体が宿主転写を変更するために使用する表遺伝子機構を調査する.
主な方法:
- Listeria monocytogenes感染中にSIRT2の核への転移を研究した.
- 遺伝子転写開始部位とSIRT2の関連性を調査した.
- 分析されたヒストンH3ライシン18 (H3K18) の脱酸化.
- SIRT2活性抑制とSIRT2ノックアウト (SIRT2-/-) を利用したマウスモデル.
主要な成果:
- Listeria monocytogenesの感染は,細菌因子InlBに依存するSIRT2の核転位を誘発する.
- SIRT2は,感染中に抑制された遺伝子の転写開始部位と関連しています.
- SIRT2はヒストンH3をライシン18 (H3K18) に deacetylatesする.
- SIRT2の活性を阻害したり,SIRT2-/-マウスを使用したりすると,細菌感染が著しく悪化します.
結論:
- SIRT2媒介によるH3K18脱酸化は,Listeria monocytogenes感染において極めて重要です.
- 病原性細菌は,宿主細胞を制御するために,SIRT2経由で表遺伝的再プログラムを利用する.
- この研究は,病原菌によって課せられた新しい表遺伝的メカニズムを明らかにしています.
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