Defects in the secretory pathway and high Ca2+ induce multiple P-bodies
Cornelia Kilchert1, Julie Weidner, Cristina Prescianotto-Baschong
1Biozentrum, Growth and Development, University of Basel, CH-4056 Basel, Switzerland.
Molecular Biology of the Cell
|June 4, 2010
Summary
Cellular stress bodies (PBs) increase with secretory pathway and calcium signaling disruptions, not just starvation. Stress type, not severity, dictates PB formation, which occurs at the endoplasmic reticulum.
Area of Science:
- Cell Biology
- Molecular Biology
- Yeast Genetics
Background:
- Cytoplasmic processing bodies (PBs) are key sites for mRNA regulation and turnover.
- PB formation is typically induced by cellular stresses like starvation or oxidative damage.
Purpose of the Study:
- To investigate novel inducers of PB formation in Saccharomyces cerevisiae.
- To elucidate the signaling pathways and cellular localization involved in stress-induced PB assembly.
Main Methods:
- Genetic analysis of Saccharomyces cerevisiae mutants (Arf1, secretory pathway).
- Induction of cellular stress (osmotic, Ca(2+) levels).
- Microscopy to observe PB number and localization, and biochemical assays for PB components.
Main Results:
- Secretory pathway mutants and Arf1 GTPase mutants significantly increased PB numbers, distinct from starvation/oxidative stress.
- Extracellular Ca(2+) mimicked this increase, while intracellular Ca(2+) depletion reduced it in secretory mutants.
- PB formation under these conditions required specific components (Pat1, Scd6) and calmodulin, suggesting distinct stress pathways.
- PB assembly was consistently observed at the endoplasmic reticulum (ER), irrespective of the stressor.
Conclusions:
- Cellular stress responses involving the secretory pathway and calcium signaling trigger PB formation through distinct mechanisms.
- PB assembly is spatially coordinated with the ER, suggesting localized mRNA regulation.
- Intracellular signals and stress type are critical determinants of PB number during cellular stress.
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