Translation arrest is a part of the cellular stress response that decreases energy consumption and enables rapid reprioritisation of gene expression. Often translation arrest leads to condensation of untranslated messenger ribonucleoproteins (mRNPs) into stress granules (SGs). Studies into mechanisms of SG formation and functions are complicated because various types of stress cause formation of SGs with different properties and composition. In this work, we focused on the mechanism of SG formation triggered by UV damage. We demonstrate that UV-induced inhibition of translation does not involve inhibition of the mechanistic target of rapamycin (mTOR) signaling or dissociation of the 48S preinitiation complexes. The general control non-derepressible 2 (GCN2; also known as EIF2AK4) kinase contributes to UV-induced SG formation, which is independent of the phosphorylation of the eukaryotic translation initiation factor 2α. Like many other types of SGs, condensation of UV-induced granules requires the Ras-GTPase-activating protein SH3-domain-binding protein 1 (G3BP1). Our work reveals that, in UV-treated cells, the mechanisms of translation arrest and SG formation may be unlinked, resulting in SGs that do not contain the major type of polysome-free preinitiation complexes that accumulate in the cytoplasm.

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翻译停滞是细胞应激反应的一部分，可减少能量消耗并能够快速重新确定基因表达的优先顺序。翻译停滞通常会导致未翻译的信使核糖核蛋白 (mRNP) 凝结成应激颗粒 (SG)。由于不同类型的应力会导致具有不同性质和组成的SG的形成，因此对SG形成和功能的机制的研究是复杂的。在这项工作中，我们重点研究了紫外线损伤引发的SG形成机制。我们证明，紫外线诱导的翻译抑制并不涉及雷帕霉素靶标 (mTOR) 信号传导的抑制或 48S 前起始复合物的解离。一般控制非去阻遏蛋白 2（GCN2；也称为 EIF2AK4）激酶有助于紫外线诱导的 SG 形成，该形成独立于真核翻译起始因子 2α 的磷酸化。与许多其他类型的 SG 一样，紫外线诱导颗粒的凝结需要 Ras-GTP 酶激活蛋白 SH3 结构域结合蛋白 1 (G3BP1)。我们的工作表明，在紫外线处理的细胞中，翻译停滞和 SG 形成的机制可能是不相关的，导致 SG 不包含在细胞质中积累的主要类型的无多核糖体预起始复合物。

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