MOF アセチルトランスファーゼはミトコンドリアの転写と呼吸を調節する

Aindrila Chatterjee¹, Janine Seyfferth², Jacopo Lucci²

¹Max Planck Institute of Immunobiology and Epigenetics, 79108 Freiburg, Germany; Faculty of Biology, Albert Ludwigs University of Freiburg, 79085 Freiburg, Germany.

Cell

|October 22, 2016

まとめ

MYSTと相互作用するタンパク質MOFはミトコンドリアに存在し,核とミトコンドリアの両方の細胞呼吸と遺伝子発現を調節する. エピジェネティクスと代謝を結びつける深刻な心臓障害を引き起こします

科学分野:

分子生物学
エピジェネティクス
細胞の代謝

背景:

エピジェネティック・レギュレータと代謝制御は相互作用し,環境の変化に細胞の反応を適応させます.
MYSTファミリーのアセチルトランスフェラーゼMOF (男性特異的な女性発現の致命的脱線) は,既知の核タンパク質である.

研究の目的:

細胞代謝におけるMOFの役割とその核の外部における潜在的局所化を調査する.
ミトコンドリア機能に対するMOFの影響と,表遺伝子調節との関連を理解する.

主な方法:

ミトコンドリアのMOF局所化を検出するための免疫光と生化学的測定法.
核およびミトコンドリアDNA (mtDNA) の遺伝子発現の分析.
Mof条件ノックアウトマウスにおける酸化リン酸化と心臓機能の評価

主要な成果:

MOFとその複雑なパートナーはミトコンドリアに局所されています.
MOFは核およびmtDNAからの呼吸器遺伝子発現を制御することによって酸化リン酸化を調節する.
MOFはmtDNAに結合し,KANSL3に依存しています.
MOFが欠けているマウスは,高縮性心筋病症とミトコンドリア変性を含む重度の心不全を示します.

結論:

MOFは核およびミトコンドリアゲノムの両方の二重転写レギュレータとして機能する.
MOFは表遺伝的メカニズムと代謝制御を結びつけ,特に高エネルギー消費組織に作用する.
ミトコンドリアMOFは心臓機能と細胞呼吸を維持するために不可欠です.

キーワード:

ハット KANSL1 について KANSL2 について KANSL3 についてカット KAT8 について KIAA1267 MOF について MSL1v1 MYST1 についてオックスフォスアセチル化エピジェネティクス心臓ミトコンドリア mtDNA について呼吸するトランスクリプション

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