Rous・サルコマ・プロウィルスにおけるフレームシフトおよび内遺伝的サプレッサー変異は,srcが2つのタンパク質をコードしていることを示唆している
Cell
|March 1, 1983
まとめ
Rous サルコマウイルスの src 遺伝子の2つの変異を分析した. フレームシフト変異は逆転を引き起こし,複製はそれを抑制し,SRCタンパク質合成を復元した.
科学分野:
- 分子生物学は分子生物学である.
- ウイルス学 ウイルス学 ウイルス学
- がん研究 がん研究
背景:
- ラット細胞のルース・サルコマウイルス (RSV) 変異により,表型の変化が生じます.
- src遺伝子変異の分析は,ウイルス腫瘍発生を理解するために重要である.
研究 の 目的:
- RSVで変形したラット細胞におけるフェノタイプの逆転と再変異の分子メカニズムを調査する.
- これらの細胞変化に起因する src 遺伝子内の変異を特徴付けるため.
主な方法:
- リバータントおよびリトランスフォーメーションされた細胞系からクローンされたプロウイルスDNAの核酸配列解析.
- 分子重量 (kd) の推定値を用いた src タンパク質製品の分析.
主要な成果:
- リバータント線000の src 遺伝子に単一の塩基対を挿入すると,フレームシフト変異が起こり,18kDの断片化された src タンパク質が生成されます.
- 再変換された線000*で242bpの重複がフレームシフトを修正し,68kd srcタンパク質の合成を可能にしました.
- 両方の細胞系は,内部AUGから開始された43 kd srcタンパク質を生成し,同じmRNAから独立した翻訳開始を示唆しました.
結論:
- srcのフレームシフト変異は,タンパク質製品を変化させることで,フェノタイプの逆転につながる可能性があります.
- 複製はフレームシフト変異を抑制し,機能的なSRCタンパク質と再変異を復元することができます.
- RSV src遺伝子は,代替翻訳開始部位と読み取りフレームを通じて複数のタンパク質同型を生成することができます.
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