ArticleNature communications2024
Nucleolar stress induces nucleolar stress body formation via the NOSR-1/NUMR-1 axis in Caenorhabditis elegans.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- rRNA intermediates associate with nucleolar reshaping in C. elegans.Nucleic acids research · 2026Article
- Hookworm genes encoding intestinal excreted-secreted proteins are transcriptionally upregulated in response to the host's immune system.PLoS neglected tropical diseases · 2026Article
- Autophagy activator AA-20 improves proteostasis and extendsProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Differential effect of ubiquitous and germline depletion of Integrator complex function on C. elegans physiology.Biology open · 2025Article
- ETS1-Driven Nucleolar Stress Orchestrates OLR1Human mutation · 2025Article
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Authors and funding
13 authors.
Funding
Abstract
Environmental stimuli not only alter gene expression profiles but also induce structural changes in cells. How distinct nuclear bodies respond to cellular stress is poorly understood. Here, we identify a subnuclear organelle named the nucleolar stress body (NoSB), the formation of which is induced by the inhibition of rRNA transcription or inactivation of rRNA processing and maturation in C. elegans. NoSB does not colocalize with other previously described subnuclear organelles. We conduct forward genetic screening and identify a bZIP transcription factor, named nucleolar stress response-1 (NOSR-1), that is required for NoSB formation. The inhibition of rRNA transcription or inactivation of rRNA processing and maturation increases nosr-1 expression. By using transcriptome analysis of wild-type animals subjected to different nucleolar stress conditions and nosr-1 mutants, we identify that the SR-like protein NUMR-1 (nuclear localized metal responsive) is the target of NOSR-1. Interestingly, NUMR-1 is a component of NoSB and itself per se is required for the formation of NoSB. We conclude that the NOSR-1/NUMR-1 axis likely responds to nucleolar stress and mediates downstream stress-responsive transcription programs and subnuclear morphology alterations in C. elegans.
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Registered trials
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