RETRACTED: TAF1は,ヒストンH2Bにおけるセリン33のリン酸化によって転写を活性化します

Tobias Maile¹, Simona Kwoczynski, Rebeccah J Katzenberger

¹Department of Biochemistry, University of California-Riverside, Riverside, CA 95121, USA.

Science (New York, N.Y.)

|May 15, 2004

まとめ

TAF1 CTKによるSer33でのヒストロンH2Bのリン酸化は,細胞サイクルと発達に関与する遺伝子の活性化に不可欠です. この変異は,ドロソフィラ菌の転写活性化に不可欠である.

科学分野:

分子生物学は分子生物学である.
エピジェネティクスエピジェネティクス
遺伝子規制遺伝子規制

背景:

ヒストンの翻訳後の改変によって引き起こされるダイナミックな染色体構造の変化は,真核細胞の転写調節に不可欠である.
リン酸化を含むヒストンの改変は,遺伝子発現に影響を与える重要な表遺伝子マークです.
TFIID複合体は,トランスクリプション開始において中心的な役割を果たします.

研究の目的:

Ser33 (H2B-S33) でヒストンH2Bのリン酸化に責任を負うキナーゼを特定する.
転写活性化におけるH2B-S33のリン酸化の役割を調査する.
開発中の遺伝子調節におけるTAF1CTKの機能的重要性を明らかにする.

主な方法:

Drosophila melanogasterをモデル生物として利用しました.
TAF1のカルボキシル末端キナーゼ領域 (CTK) の酵素活性を調べました.
分子生物学技術を使用して,遺伝子発現に関連したH2B-S33のリン酸化レベルを分析しました.

主要な成果:

特定されたTAF1CTKは,Ser33 (H2B-S33) でヒストンH2Bをリン酸化するキナーゼである.
H2B-S33のリン酸化が細胞サイクルとセグメンテーション遺伝子の転写活性化と相関していることが観察されました.
TAF1 CTKの活性が低下すると,H2B-S33のリン酸化が低下し,転写活性化が低下することが示された.

結論:

H2B-S33は,TAF1 CTKの生理学的基板である.
TAF1 CTKによるH2B-S33のリン酸化は,転写の活性化に不可欠である.
この経路は,ドロソフィラの細胞サイクル進行と胚の発達に不可欠です.

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