The environmental stress response regulates ribosome content in cell cycle-arrested S. cerevisiae.
The environmental stress response regulates ribosome content in cell cycle-arrested S. cerevisiae.
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DOI：
10.3389/fcell.2023.1118766
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发表时间：
2023
影响因子：
5.5
通讯作者：
中科院分区：
文献类型：
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作者：
细胞周期阻滞的延长在分化细胞中自然发生，是对各种应激（如营养剥夺或化疗药物治疗）的反应。细胞是否以及如何在延长的细胞周期停滞中存活尚不清楚。在这里，我们使用酿酒酵母比较生理细胞周期阻滞和基因诱导阻滞在G1期、中期和后期。在所有研究条件下，延长的细胞周期阻滞导致生长衰减，与环境应激反应（ESR）的激活相一致，并且通过全核糖体纯化和TMT质谱测定核糖体含量降低。通过Ras/PKA通路的过度激活抑制ESR，在长时间的阻滞过程中降低了细胞活力，证明了ESR的细胞保护作用。在被阻滞的人类细胞系中，细胞生长的衰减和应激诱导的信号通路的激活也会发生，这提高了对延长细胞周期阻滞的反应是保守的可能性。
Prolonged cell cycle arrests occur naturally in differentiated cells and in response to various stresses such as nutrient deprivation or treatment with chemotherapeutic agents. Whether and how cells survive prolonged cell cycle arrests is not clear. Here, we used S. cerevisiae to compare physiological cell cycle arrests and genetically induced arrests in G1-, meta- and anaphase. Prolonged cell cycle arrest led to growth attenuation in all studied conditions, coincided with activation of the Environmental Stress Response (ESR) and with a reduced ribosome content as determined by whole ribosome purification and TMT mass spectrometry. Suppression of the ESR through hyperactivation of the Ras/PKA pathway reduced cell viability during prolonged arrests, demonstrating a cytoprotective role of the ESR. Attenuation of cell growth and activation of stress induced signaling pathways also occur in arrested human cell lines, raising the possibility that the response to prolonged cell cycle arrest is conserved.
影响因子：
9.2
作者：
Goranov, Alexi I.;Gulati, Amneet;Dephoure, Noah;Takahara, Terunao;Maeda, Tatsuya;Gygi, Steven P.;Manalis, Scott;Amon, Angelika
通讯作者：
Amon, Angelika