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ER tethering and active transport govern condensate diffusion during hyperosmotic stress
Bisal Halder1,2, Guoming Gao1,3, Armin Ahnoud1,4
1Center for RNA Biomedicine, University of Michigan, Ann Arbor, MI, 48109, USA.
Genome Biology
|March 25, 2026
Summary
Hyperosmotic shock causes cell compression, leading to biomolecular condensates. These condensates exhibit sub-diffusion due to ER attachment and super-diffusion via active transport, not physical barriers.
Area of Science:
- Cell Biology
- Biophysics
Background:
- Hyperosmotic shock causes cell volume compression, inducing hyperosmotic phase separation (HOPS) condensates.
- The diffusion dynamics and mechanisms of HOPS condensates in compressed cells are poorly understood.
Purpose of the Study:
- To characterize the diffusion dynamics of HOPS condensates in hyperosmotically compressed cells.
- To elucidate the underlying mechanisms governing condensate mobility.
Main Methods:
- Live-cell fluorescent single-particle tracking (SPT) of model protein DCP1A condensates.
- Spatial accessibility measurements and organelle labeling.
- Tracking of genetically encoded multimeric nanoparticles (GEMs).
Main Results:
- HOPS condensates primarily exhibit sub-diffusion, with a fraction showing super-diffusion.
- Sub-diffusion is linked to endoplasmic reticulum (ER) attachment; super-diffusion involves microtubule-dependent transport.
- Cytoplasm remains accessible via diffusion, indicating interactions, not physical corralling, restrict condensate mobility.
Conclusions:
- Cytosol remains dynamic during hyperosmotic compression, challenging previous views.
- Condensate mobility is spatially organized by docking to membrane structures and active transport.
- This provides a framework for understanding condensate spatiotemporal organization in stressed cells.
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