图1. 哺乳动物与植物细胞核糖体应激及DNA损伤反应途径比较
核糖体蛋白突变或核糖体生物发生缺陷会导致核糖体应激。在哺乳动物细胞中, 核糖体应激和DNA损伤反应均由p53响应。正常情况下, p53与E3泛素连接酶MDM2相互作用, 通过泛素降解途径调控其蛋白稳态; 当核糖体应激发生时, 一部分RPs从核仁中释放出来, 与MDM2的酸性结构域结合, 降低其对p53的作用。p53作为转录因子介导下游细胞周期阻滞、细胞衰老及凋亡。在植物中, 类p53转录因子SOG1被ATM和ATR激活并磷酸化, 参与DNA损伤反应, 但是目前尚无证据表明SOG1在核糖体应激响应中发挥作用。而另一个NAC家族转录因子ANAC082可能参与一定的核糖体应激反应。实线箭头表示正常状态, 虚线箭头表示应激状态。

Figure 1. Comparison of ribosomal stress and DNA damage response pathways between mammalian and plant cells
Ribosomal stress can be resulted from mutations in genes encoding ribosomal proteins or defects in ribosome biogenesis. In mammalian cells, both ribosomal stress and DNA damage responses are mediated by p53. Under normal conditions, p53 interacts with E3 ubiquitin ligase MDM2, which regulates its protein homeostasis through ubiquitin degradation pathway; when ribosomal stress occurs, some RPs are released from the nucleolus and bind to the acidic domain of MDM2, leading to reduction of its effect on p53. p53 acts as a transcription factor to mediate downstream cell cycle arrest, cell aging and apoptosis. In plants, SOG1, a p53-like transcription factor that can be activated and phosphorylated by ATM and ATR, is involved in DNA damage response, but no evidence shows its involvement in ribosomal stress response. However, another NAC transcription factor, ANAC082, is reported to be involved in ribosomal stress response. Solid arrow indicates the normal state, the dotted arrows indicate stress state.