ArticleThe Journal of biological chemistry2015
Intracellular Bacterial Pathogens Trigger the Formation of U Small Nuclear RNA Bodies (U Bodies) through Metabolic Stress Induction.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 40 citations in OpenAlex.
- Biphasic SMN condensates safeguard stress-induced cytoplasmic mislocalization of splicing RNPs.Cellular and molecular life sciences : CMLS · 2026Article
- Article
- Stress-induced proteins enhance thermal endurance in soil bacterium Priestia aryabhattai strain PSK.N2.Antonie van Leeuwenhoek · 2025Article
- Enhanced packaging of U6 small nuclear RNA and splicing-related proteins into extracellular vesicles during HIV infection.Science advances · 2025Article
- Cytosolic retention of HtrA2 during mitochondrial protein import stress triggers the DELE1-HRI pathway.Communications biology · 2024Article
- Large Stokes shift fluorescent RNAs for dual-emission fluorescence and bioluminescence imaging in live cells.Nature methods · 2023Article
- Brucella effectors NyxA and NyxB target SENP3 to modulate the subcellular localisation of nucleolar proteins.Nature communications · 2023Article
- A bacterial virulence factor interacts with the splicing factor RBM5 and stimulates formation of nuclear RBM5 granules.Scientific reports · 2022Article
- Microbiota and Transcriptomic Effects of an Essential Oil Blend and Its Delivery Route Compared to an Antibiotic Growth Promoter in Broiler Chickens.Microorganisms · 2022Article
- LncRNAs divide and rule: The master regulators of phase separation.Frontiers in genetics · 2022Review
- Advances in the phase separation-organized membraneless organelles in cells: a narrative review.Translational cancer research · 2021Review
- A multicolor riboswitch-based platform for imaging of RNA in live mammalian cells.Methods in enzymology · 2020Article
- The heme-regulated inhibitor is a cytosolic sensor of protein misfolding that controls innate immune signaling.Science (New York, N.Y.) · 2019Article
- Isoginkgetin, a Natural Biflavonoid Proteasome Inhibitor, Sensitizes Cancer Cells to Apoptosis via Disruption of Lysosomal Homeostasis and Impaired Protein Clearance.Molecular and cellular biology · 2019Article
- Human Intestinal Enteroids as a Model System ofInfection and immunity · 2019Article
- A multicolor riboswitch-based platform for imaging of RNA in live mammalian cells.Nature chemical biology · 2018Article
- UsnRNP biogenesis: mechanisms and regulation.Chromosoma · 2017Review
- SMN regulation in SMA and in response to stress: new paradigms and therapeutic possibilities.Human genetics · 2017Review
- Activating transcription factor 4 underlies the pathogenesis of arsenic trioxide-mediated impairment of macrophage innate immune functions.Toxicology and applied pharmacology · 2016Article
- The transcriptional and splicing landscape of intestinal organoids undergoing nutrient starvation or endoplasmic reticulum stress.BMC genomics · 2016Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Invasive bacterial pathogens induce an amino acid starvation (AAS) response in infected host cells that controls host defense in part by promoting autophagy. However, whether AAS has additional significant effects on the host response to intracellular bacteria remains poorly characterized. Here we showed that Shigella, Salmonella, and Listeria interfere with spliceosomal U snRNA maturation in the cytosol. Bacterial infection resulted in the rerouting of U snRNAs and their cytoplasmic escort, the survival motor neuron (SMN) complex, to processing bodies, thus forming U snRNA bodies (U bodies). This process likely contributes to the decline in the cytosolic levels of U snRNAs and of the SMN complex proteins SMN and DDX20 that we observed in infected cells. U body formation was triggered by membrane damage in infected cells and was associated with the induction of metabolic stresses, such as AAS or endoplasmic reticulum stress. Mechanistically, targeting of U snRNAs to U bodies was regulated by translation initiation inhibition and the ATF4/ATF3 pathway, and U bodies rapidly disappeared upon removal of the stress, suggesting that their accumulation represented an adaptive response to metabolic stress. Importantly, this process likely contributed to shape the host response to invasive bacteria because down-regulation of DDX20 expression using short hairpin RNA (shRNA) amplified ATF3- and NF-κB-dependent signaling. Together, these results identify a critical role for metabolic stress and invasive bacterial pathogens in U body formation and suggest that this process contributes to host defense.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.