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PRAG1 Condensation Drives Cell Contraction Under Stress
Peiwu Ye1, Peiran Jiang2,3, Luyu Ye4
1Institute of Chinese Medical Sciences, University of Macau, Macau 999078, China.
Biomolecules
|March 28, 2025
Summary
Pseudopodium-enriched atypical kinase 1 (PRAG1) forms dynamic cell condensates. These PRAG1 condensates drive cell contraction, particularly under stress, revealing a new mechanism linked to Parkinson
Area of Science:
- Cell Biology
- Molecular Mechanisms
- Neuroscience
Background:
- Pseudopodium-enriched atypical kinase 1 (PRAG1), a pseudokinase, is implicated in cell morphology regulation.
- The precise molecular mechanism underlying PRAG1's role in cell morphology remains unclear.
Purpose of the Study:
- To elucidate the molecular mechanism by which PRAG1 regulates cell morphology.
- To investigate the role of PRAG1 in cellular condensation and contraction under stress conditions.
Main Methods:
- Investigated PRAG1's ability to form dynamic cellular condensates.
- Utilized condensate-formation-deficient PRAG1 mutants to assess functional significance.
- Observed PRAG1 condensate formation in various stress models and patient-derived neurons.
Main Results:
- PRAG1 forms dynamic condensates in cells, mediated by its αN and αJ helices.
- PRAG1 condensates are essential for mediating cell contraction; mutants lacking this function lose the ability.
- Spherical PRAG1 condensates are observed in diverse stress models and Parkinson's disease patient-derived dopaminergic neurons.
Conclusions:
- PRAG1 condensation drives cell contraction, establishing a novel mechanism for morphological regulation.
- Aberrant PRAG1 phase separation may be linked to stress-induced cell contraction.
- Findings suggest a potential role for PRAG1 in Parkinson's disease pathogenesis.
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