プロラクチン媒介によるカゼイン遺伝子発現の転写および転写後の制御

W A Guyette, R J Matusik, J M Rosen

Cell

|August 1, 1979

まとめ

プロラクチンは,転写を促進し,mRNAの安定性を劇的に拡張することによって,カゼインmRNAレベルを大幅に増加させます. この二重作用は,乳腺の効率的な乳タンパク質生産を保証します.

科学分野:

分子内分泌学分子内分泌学
遺伝子発現の規制について
哺乳類生理学哺乳類生理学について

背景:

プロラクチンは,乳腺の機能を調節する重要なペプチドホルモンです.
カゼイン遺伝子発現を理解することは,授乳を研究する上で極めて重要です.

研究の目的:

プロラクチンがカゼイン遺伝子発現に及ぼす規制メカニズムを解明する.
トランスクリプションおよびポストトランスクリプションイベントの貢献を決定する.

主な方法:

乳腺臓器培養を用いた.
プロラクチンは,その効果を評価するために追加されました.
カゼインmRNAの転写率と半減期を測定した.
比較のために,ポリ (A) RNAの半減期を評価した.

主要な成果:

プロラクチンは1時間以内にカゼインmRNAの転写を2〜4倍に増加させた.
プロラクチンはカゼインmRNAの半減期を17~25倍に増加させた.
これらの効果の組み合わせが,カゼインmRNAの蓄積を説明する.
プロラクチンは,ポリ (A) RNAの半減期に最小限の影響を及ぼしました.

結論:

プロラクチンは,トランスクリプションおよびポストトランスクリプションの両方のメカニズムを通じてカゼイン遺伝子発現を調節します.
mRNAの安定性の向上は,プロラクチン誘発によるカゼイン蓄積の主要な要因である.
ホルモンの調節には,複数の遺伝子発現レベルでの協調反応が伴う.

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