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. 2022 Dec 1:9:1066650.
doi: 10.3389/fmolb.2022.1066650. eCollection 2022.

The enigma of ultraviolet radiation stress granules: Research challenges and new perspectives

Alexandra J Cabral  1 , Danielle C Costello  1 , Natalie G Farny  1
Affiliations

The enigma of ultraviolet radiation stress granules: Research challenges and new perspectives

Alexandra J Cabral et al. Front Mol Biosci. .

Abstract

Stress granules (SGs) are non-membrane bound cytoplasmic condensates that form in response to a variety of different stressors. Canonical SGs are thought to have a cytoprotective role, reallocating cellular resources during stress by activation of the integrated stress response (ISR) to inhibit translation and avoid apoptosis. However, different stresses result in compositionally distinct, non-canonical SG formation that is likely pro-apoptotic, though the exact function(s) of both SGs subtypes remain unclear. A unique non-canonical SG subtype is triggered upon exposure to ultraviolet (UV) radiation. While it is generally agreed that UV SGs are bona fide SGs due to their dependence upon the core SG nucleating protein Ras GTPase-activating protein-binding protein 1 (G3BP1), the localization of other key components of UV SGs are unknown or under debate. Further, the dynamics of UV SGs are not known, though unique properties such as cell cycle dependence have been observed. This Perspective compiles the available information on SG subtypes and on UV SGs in particular in an attempt to understand the formation, dynamics, and function of these mysterious stress-specific complexes. We identify key gaps in knowledge related to UV SGs, and examine the unique aspects of their formation. We propose that more thorough knowledge of the distinct properties of UV SGs will lead to new avenues of understanding of the function of SGs, as well as their roles in disease.

Keywords: biomolecular condensation; cell cycle; neurodegeneration; poly(A)+ RNA; stress granules; ultraviolet radiation (UV).

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
Composition and formation of UV SGs. (A) RACK1 does not localize to UV-induced SGs. U2OS treated with arsenite (500 μM, left panels) or UV (15 J/m2, then assayed at 4 h post-UV, right panels) and co-stained with antibodies to G3BP1 and RACK1. Profile intensity plots over the red line from each image were compiled using ImageJ. (B) U2OS treated with arsenite (500 μM, left panels) or UV (15 J/m2, then assayed at 4 h post-UV, right panels) and co-stained with antibodies to G3BP1 and Oligo (dT). Profile intensity plots over the red line from each image were compiled using ImageJ. (C) Poly(A)+ RNA SGs can form after UV treatment. U2OS were untreated or treated with UV (15 J/m2) for 3 h, then arsenite (500 µM) was added where indicated for a 1 h, then cells were fixed and co-stained with antibodies to G3BP1 and Oligo (dT) FISH. Red arrows point to prominent SGs in each treatment condition. (D) HaCaT cells do not form UV SGs. HaCaT cells were exposed to arsenite 250 µM for 1 h, or exposed to 3,000 J/m2 UV (4 h post-exposure), then stained with antibody for G3BP1 to assess SG formation. Detailed methods for all panels are available as Supplementary Material online. (E) A model for UV SG suppression. See Discussion section for details.
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