SETD2による二重染色体と細胞骨格の改造
In Young Park1, Reid T Powell1, Durga Nand Tripathi1
1Center for Translational Cancer Research, Institute of Biosciences and Technology, Texas A&M Health Science Center, Houston, TX 77030, USA.
Cell
|August 13, 2016
まとめ
ヒストンメチルトランスフェラーゼSETD2は微小管をメチル化し,チューブリンとヒストンのコードの両方のゲノム安定性と完全性を維持する二重の役割を果たしています.
科学分野:
- 細胞生物学
- エピジェネティクス
- 分子生物学
背景:
- 翻訳後の修正 (PTM) は,異なる
- コード
- 細胞機能を制御する チューブリンとヒストンの
- これらのコードを制御する分子機構は,特に
- 作家たち
- そして
- 消しゴム
- 細胞骨とエピジェノームは別々に検討された.
- アセチル化を含む微小管のPTMは,特殊な細胞機能に不可欠である.
研究 の 目的:
- 微小管変異におけるヒストンメチルトランスファーゼの役割を調査する.
- ヒストンメチルトランスフェラーゼであるSETD2がチューブリンを変化させるかどうかを判断する.
- 細胞過程におけるチューブリンメチル化の機能を明らかにする.
主な方法:
- 質量スペクトロメトリを用いてチューブリンメチル化を特定した.
- 細胞モデルでSETD2の遺伝子消去を用いた.
- ミトーシス,シトキネシス,ゲノム安定性を含む観察された細胞現象型.
主要な成果:
- 動的微小管のPTMとしてメチル化が確認された.
- SETD2はライシン40でα-チューブリンをメチル化する.
- SETD2の削除は,ミトーシス,シトキネシス,ゲノム不安定性 (マイクロ核,ポリプロイド性) の欠陥につながる.
結論:
- SETD2は,クロマチン (ヒストン) と細胞骨格 (チューブリン) を両方メチル化する二重機能酵素である.
- SETD2による微小管のメチル化は,ミトーシス・スパインドルとシトキネシスの完全性にとって不可欠である.
- この研究は,チューブリンメチル化がゲノムの安定性およびチューブリンとヒストンのコードの調整に必要であることを明らかにしています.
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