G3BP1 promotes stress-induced RNA granule interactions to preserve polyadenylated mRNA

Aulas, Anaïs; Caron, Guillaume; Gkogkas, Christos G.; Mohamed, Nguyen‐Vi; Destroismaisons, Laurie; Sonenberg, Nahum; Leclerc, Nicole; Parker, J. Alex; Velde, Christine Vande

doi:10.1083/jcb.201408092

Cited by 96 publications

(98 citation statements)

References 48 publications

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“…This notion is supported by functional studies showing that depletion of SG-inducing proteins decreases mRNA levels globally, consistent with reduced mRNA stability [105, 106]. However, it is important to keep in mind that SGs may, instead, be a consequence of translation repression rather than a cause of translational repression.…”

Section: Stress Granules and Rna Degradationmentioning

confidence: 87%

Stress and the nonsense-mediated RNA decay pathway

Goetz

Wilkinson

2017

Cell. Mol. Life Sci.

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Cells respond to internal and external cellular stressors by activating stress response pathways that re-establish homeostasis. If homeostasis is not achieved in a timely manner, stress pathways trigger programmed cell death (apoptosis) to preserve organism integrity. A highly-conserved stress pathway is the unfolded protein response (UPR), which senses excessive amounts of unfolded proteins in the ER. While a physiologically beneficial pathway, the UPR requires tight regulation to provide a beneficial outcome and avoid deleterious consequences. Recent work has demonstrated that a conserved and highly selective RNA degradation pathway—Nonsense-Mediated RNA Decay (NMD)—serves as a major regulator of the UPR pathway. NMD degrades mRNAs encoding UPR components to prevent UPR activation in response to innocuous ER stress. In response to strong ER stress, NMD is inhibited by the UPR to allow for a full-magnitude UPR response. Recent studies have indicated that NMD also has other stress-related functions, including promoting the timely termination of the UPR to avoid apoptosis; NMD also regulates responses to non-ER stressors, including hypoxia, amino-acid deprivation, and pathogen infection. NMD regulates stress responses in species across the phylogenetic scale, suggesting it has conserved roles in shaping stress responses. Stress pathways are frequently constitutively activated or dysregulated in human disease, raising the possibility that “NMD therapy” may provide clinical benefit by downmodulating stress responses.

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Section: Stress Granules and Rna Degradationmentioning

confidence: 87%

Stress and the nonsense-mediated RNA decay pathway

Goetz

Wilkinson

2017

Cell. Mol. Life Sci.

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“…The stress granule protein G3BP1 is regulated by TDP-43 (Aulas et al, 2012;McDonald et al, 2011) and is essential for stress granule-processing body docking (Aulas et al, 2015).…”

Section: Alterations In the Proteasome System Promotes Ervk Viral Promentioning

confidence: 99%

TDP-43 regulates endogenous retrovirus-K viral protein accumulation

Manghera

Ferguson-Parry

Douville

2016

Neurobiology of Disease

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“…Interestingly, most SIC-bound RNA-binding proteins were also found amongst our previously characterized Sam68 ribonucleoparticles (RNPs) (Huot et al, 2009b). These RNPs were shown to affect both focal adhesion turnover and cellular spreading (Huot et al, 2009a), and have the ability to modulate mRNA translation (Aulas et al, 2015;Huot et al, 2009b;Klein et al, 2013;Mazroui et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Localized translation regulates cell adhesion and transendothelial migration

Bergeman

Caillier

Houle

et al. 2016

Journal of Cell Science

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Epithelial-to-mesenchymal transition (EMT) is a process by which cancer cells gain the ability to leave the primary tumor site and invade surrounding tissues. These metastatic cancer cells can further increase their plasticity by adopting an amoeboid-like morphology, by undergoing mesenchymal-to-amoeboid transition (MAT). We found that adhering cells produce spreading initiation centers (SICs), transient structures that are localized above nascent adhesion complexes, and share common biological and morphological characteristics associated with amoeboid cells. Meanwhile, spreading cells seem to return to a mesenchymal-like morphology. Thus, our results indicate that SIC-induced adhesion recapitulates events that are associated with amoeboid-to-mesenchymal transition (AMT). We found that polyadenylated RNAs are enriched within SICs, blocking their translation decreased adhesion potential of metastatic cells that progressed through EMT. These results point to a so-farunknown checkpoint that regulates cell adhesion and allows metastatic cells to alter adhesion strength to modulate their dissemination.

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G3BP1 promotes stress-induced RNA granule interactions to preserve polyadenylated mRNA

Abstract: The TDP-43 target G3BP1 is essential for a functional interaction between stress granules and processing bodies.

Cited by 96 publications

References 48 publications

Stress and the nonsense-mediated RNA decay pathway

Stress and the nonsense-mediated RNA decay pathway

TDP-43 regulates endogenous retrovirus-K viral protein accumulation

Localized translation regulates cell adhesion and transendothelial migration

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