The phase separation of the non-membrane bound Sec bodies occurs in Drosophila S2 cells by coalescence of components of the ER exit sites under the stress of amino-acid starvation. Here we address which signaling pathways cause Sec body formation. We find that two pathways are critical. The first is a SIK dependent pathway induced by salt (NaCl) stress in a necessary and sufficient manner. The second is the activation of IRE1 (one of the key kinases mediating the Unfolded Protein Response) by absence of amino- acids, which partly leads to the depletion of intracellular ATP. However, IRE1 activation is not sufficient to induce Sec body formation and needs to be combined to salt stress. This works pioneers the role of SIK in phase transition and re-enforces the role of IRE1 as a metabolic sensor for the level of circulating amino-acids.

中文翻译：

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盐诱导的激酶激活和依赖IRE1的细胞内ATP耗竭，在果蝇细胞中形成Sec体。

在果蝇S2细胞中，非膜结合Sec体的相分离是通过在氨基酸饥饿的压力下ER出口位点的组分聚结而发生的。在这里，我们解决导致Sec身体形成的信号通路。我们发现两条途径很关键。首先是盐（NaCl）胁迫以必要和充分的方式诱导的SIK依赖性途径。第二个是由于缺少氨基酸，IRE1（介导未折叠蛋白反应的关键激酶之一）被激活，这部分导致细胞内ATP的消耗。但是，IRE1激活不足以诱导Sec体形成，需要结合盐胁迫。这项工作开拓了SIK在相变中的作用，并增强了IRE1作为循环氨基酸水平代谢传感器的作用。