氧化应激重新编程转录协激活剂Yki,以抑制细胞增殖
Xiaohan Sun1, Dafa Zhou2, Yuanfei Sun2
1Key Laboratory of Biodiversity Conservation and Bioresource Utilization of Jiangxi Province, College of Life Sciences, Jiangxi Normal University, Nanchang 330022, China; School of Life Sciences and Medicine, Shandong University of Technology, Zibo 255000, China.
Cell reports
|August 6, 2024
概括
氧化应激重新编程约基 (Yki) 从促进细胞增殖到通过改变其结合伙伴来抑制细胞增殖. 这种机制对于Drosophila在压力下生存至关重要.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 遗传学 是一个遗传学.
背景情况:
- 转录协活性剂Yorkie (Yki) 是通过促进细胞增殖来调节器官大小的关键调节剂.
- 在细胞应激下控制Yki活动的精确机制,例如氧化应激,仍然在很大程度上是未知的.
研究的目的:
- 为了阐明细胞如何调节约克 (Yki) 活动以应对氧化应激.
- 确定参与Yki介导细胞对氧化应激反应的分子参与者和机制.
主要方法:
- 在氧化应激条件下,研究了Yki,Scaloped (Sd) 和叉盒O (Foxo) 之间的蛋白质-蛋白质相互作用.
- 利用分子生物学技术分析与增殖和应激反应相关的基因表达变化.
- 评估了Usp7在Foxo脱化中的作用及其随后与Yki的相互作用.
- 评估了在暴露于氧化应激的Drosophila模型中Yki对生存的必要性.
主要成果:
- 氧化应激破坏了Yki-Scalloped (Sd) 复合体的形成.
- 氧化应激促进了Yki和叉盒O (Foxo) 之间的相互作用.
- Usp7对Foxo进行双化,增强其与Yki的结合亲和力,并激活增殖抑制基因.
- 在氧化应激期间,Yki对于Drosophila的生存是不可或缺的.
结论:
- 氧化应激触发了Yki功能的重编程,将其从增殖促进剂转变为增殖抑制剂.
- 这种Yki介导的重编程构成了对抗氧化损伤的关键自我保护机制.
- 这些发现揭示了细胞适应有害刺激的新途径,涉及转录因子动态.
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