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Calmodulin antagonists inhibit secretion in Paramecium.
The Journal of Cell Biology
|April 1, 1983
Summary
Calmodulin (CaM) antagonists, trifluoperazine (TFP) and W-7, reversibly inhibit calcium-dependent secretion in Paramecium by blocking trichocyst matrix expansion. These findings suggest CaM regulates exocytosis in these cells.
Area of Science:
- Cell Biology
- Biochemistry
Background:
- Secretion in Paramecium is a calcium-dependent exocytic process involving trichocysts.
- Trichocyst matrix undergoes Ca2+-induced structural reordering during expansion, with defined stages (I, II, III).
Purpose of the Study:
- To investigate the role of calmodulin (CaM) in regulating Paramecium secretion.
- To assay the effects of CaM antagonists trifluoperazine (TFP) and W-7 on trichocyst matrix expansion.
Main Methods:
- Utilized Paramecium model system to study exocytosis.
- Employed CaM antagonists TFP and W-7 to inhibit secretion.
- Conducted ultrastructural examination of trichocyst stages during inhibition.
- Used Ca2+ ionophore A23187 to assess recovery from inhibition.
Main Results:
- TFP and W-7 reversibly blocked picric acid-induced matrix release.
- Organelles were prevented from transitioning from stage I to stage II by TFP and W-7.
- High extracellular Ca2+ partially moderated TFP inhibition, but this effect was overcome by higher TFP concentrations.
- Ca2+ ionophore treatment promoted matrix expansion following TFP exposure, though residual inhibition persisted.
Conclusions:
- Calmodulin (CaM) plays a regulatory role in Paramecium secretion.
- CaM likely controls Ca2+-dependent matrix expansion during exocytosis.