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Updated: Aug 13, 2026

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Methods to Classify Cytoplasmic Foci as Mammalian Stress Granules
Published on: May 12, 2017
Temporal gating dictates stress-induced transcript export from the nucleus
Noah S Helton1,2, Benjamin Dodd1,2, Stephanie L Moon3,2
1Department of Human Genetics, University of Michigan, Ann Arbor, Michigan 48109, USA.
Genes & Development
|August 11, 2026
Summary
Nuclear mRNA export is inhibited during cellular stress. Transcriptional timing, not sequence, dictates which stress-induced mRNAs are exported from the nucleus, revealing a novel stress response mechanism.
Area of Science:
- Molecular Biology
- Cell Biology
- Genetics
Background:
- Nuclear mRNA export regulation during cellular stress is poorly understood.
- Previous research focused on transcriptional and translational control, neglecting mRNA export mechanisms.
Purpose of the Study:
- To investigate the role of regulated nuclear mRNA export in the cellular stress response.
- To determine the factors governing the export of stress-induced mRNAs from the nucleus.
Main Methods:
- Single-molecule mRNA imaging in human cells under arsenite and heat stress.
- Transcriptome-wide analyses to identify nuclear-retained and exported mRNAs.
- Reporter RNA assays to assess mRNA export competence based on transcription timing.
Main Results:
- Nuclear mRNA export is progressively inhibited during arsenite and heat stress.
- The timing of mRNA biogenesis, not sequence-specific features, governs nucleocytoplasmic distribution during stress.
- Early transcribed stress-induced mRNAs, including immediate early genes, are exported before global export inhibition.
- Later transcribed mRNAs and most stress-induced transcripts, like heat shock proteins, accumulate in the nucleus.
Conclusions:
- Cellular stress employs temporal gating of mRNA export, prioritizing early-produced transcripts.
- Transcriptional timing is the primary determinant of nuclear export efficiency for stress-induced mRNAs in human cells.
- This mechanism offers a new perspective on cellular stress response pathways.
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