推定されるタンパク質キナーゼは,S. cerevisiaeのフェロモン誘発の細胞サイクル停止を克服する

W E Courchesne¹, R Kunisawa, J Thorner

¹Department of Biochemistry, University of California, Berkeley 94720.

Cell

|September 22, 1989

まとめ

KSS1遺伝子の過剰発現は,酵母細胞がフェロモン誘発の細胞サイクル停止から回復するのを助けます. このKSS1遺伝子の機能は,他の既知の回復経路とは独立しており,WHI1遺伝子を含む.

科学分野:

分子生物学は分子生物学である.
細胞サイクル規制について
イースト遺伝学イースト遺伝学

背景:

イーストの交配フェロモンは,G1細胞サイクル停止を誘発する.
この停止からの回復には,SST2遺伝子産物とアルファ因子受容体の細胞プラズマ尾を含む特定の細胞プロセスが必要です.

研究の目的:

フェロモン誘発性停止からの酵母細胞サイクル回復におけるKSS1遺伝子の役割を調査する.
交配フェロモンに対する無敏感化に関与する新しい経路を特定する.

主な方法:

酵母変異体の遺伝子分析 (sst2変異を有するMATa細胞).
遺伝子過剰発現の研究 (KSS1遺伝子).
シトプラズマ尾を欠くアルファ因子受容体変異体の分析.
遺伝子相互作用の調査 (KSS1とWHI1).

主要な成果:

KSS1遺伝子の過剰発現は,sst2変異細胞の回復欠陥を抑制する.
また,KSS1の過剰発現は,切断されたアルファ因子受容体を持つ細胞の欠陥を救済する.
KSS1は,SST2と受容体尾から独立して作用し,無感化を促します.
KSS1の回復活動は,WHI1遺伝子に依存しており,共通の経路を示唆しています.

結論:

KSS1は,フェロモン停止からの無感化と回復のための第三の独立した経路を表すタンパク質キナーゼをコードします.
KSS1とWHI1 (サイクリンホモログ) は,共通の成長制御経路で一緒に機能する可能性が高い.

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