男性の生殖細胞におけるCREM依存転写は,キネシンによって制御される

Betina Macho¹, Stefano Brancorsini, Gian Maria Fimia

¹Institut de Génétique et de Biologie Moléculaire et Cellulaire, B. P. 10142, 67404 Illkirch, Strasbourg, France.

Science (New York, N.Y.)

|December 21, 2002

まとめ

キネシンKIF17bは,男性生殖細胞の発達中にその核の局所化を調節することによって,転写協活性化剤ACTの活動を制御する. この相互作用は,精子形成のプロセスである精子生成に極めて重要です.

科学分野:

生殖生物学生殖生物学
分子細胞生物学分子細胞生物学
精子生成の研究研究について

背景:

ACT (LIMのみのタンパク質) とCREM (転写活性化剤) は,精子生成の過程で生後遺伝子の調節に協力する.
CREMの無効化はマウスの精子生成を阻害し,CREMとACTの相互作用の重要性を強調しています.

研究の目的:

CREMとACTの機能的な相互作用を規制する規制メカニズムを特定する.
精子生成中にACTの活性がどのように制御されるかを明らかにする.

主な方法:

共同免疫プレシピテーションまたは同様の技術を使用して,タンパク質とタンパク質の相互作用を調査した.
ACTとKIF17b.の細胞内局在を決定した.
KIF17bの局所化に対するレプトミシンB (Crm1阻害剤) の効果を評価した.

主要な成果:

ACTは,雄性生殖細胞に高い発現度を持つキネシンであるKIF17bと選択的に結合する.
ACT-KIF17bの相互作用とACTの細胞内局所化は,精子形成の過程でステージに特異的です.
KIF17bの核輸出はCrm1受容体によって媒介され,レプトミシンBの感受性によって示される.

結論:

KIF17bは,その細胞内局所化を調節することによって,ACTの活動を直接制御します.
このキネシン媒介の調節は,精子生成中の遺伝子発現を制御する重要なステップです.

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