The crosstalk between cellular stress responses and innate immune signaling pathways remains poorly understood. Cells can respond to stressors by assembling stress granules that store 40S ribosomes, translation initiation factors, and mRNAs, and allow the cell to survive. Some stressors can activate the NLRP3 inflammasome, which leads to pyroptotic cell death. Stress granules and the NLRP3 inflammasome provide distinct cell fate choices to the cell. These complexes also involve distinct types of phase transitions—liquid–liquid phase separation for stress granules and prionoid phase transition for the NLRP3 inflammasome. We recently reported that DDX3X modulates this crosstalk by acting as a common essential factor for NLRP3 inflammasome activation and stress granule assembly. Here, we discuss the role of DDX3X in modulating the liquid–liquid phase separation and prionoid phase transition required for making cell fate decisions under stress conditions.

中文翻译：

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DDX3X处于液-液和类固醇相变的十字路口，可在应激细胞中决定生命和死亡细胞的命运。

细胞应激反应和先天性免疫信号通路之间的串扰仍然知之甚少。细胞可以通过组装可存储40S核糖体，翻译起始因子和mRNA的应激颗粒来应对应激源，并使细胞存活。一些应激源可以激活NLRP3炎性小体，从而导致焦细胞死亡。应激颗粒和NLRP3炎性小体为细胞提供了不同的细胞命运选择。这些复合物还涉及不同类型的相变-应力颗粒的液-液相分离和NLRP3炎性小体的类状相变。我们最近报道说，DDX3X通过充当NLRP3炎性体激活和应激颗粒组装的共同必要因素来调节这种串扰。这里，