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Published on: August 6, 2016
Cyclic ADP-ribose-gated Ca2+ release in sea urchin eggs requires an elevated
1Department of Physiology, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
The Journal of Biological Chemistry
|July 4, 1997
Summary
Cyclic ADP-ribose (cADPr) triggers slow intracellular calcium release in sea urchin eggs, requiring a rise in calcium levels for full activity. This calcium feedback mechanism is essential for cADPr-mediated calcium release.
Area of Science:
- Cellular Biology
- Biochemistry
Background:
- Cyclic ADP-ribose (cADPr) is known to mobilize intracellular calcium (Ca2+) stores.
- The precise mechanism by which cADPr initiates Ca2+ release remains unclear.
Purpose of the Study:
- To investigate the kinetics of Ca2+ release mediated by cADPr in sea urchin eggs.
- To elucidate the role of calcium concentration in cADPr-gated Ca2+ release.
Main Methods:
- Utilized caged cADPr to study Ca2+ transient kinetics in intact sea urchin eggs.
- Compared cADPr-induced Ca2+ release with that induced by caged inositol 1,4,5-trisphosphate.
- Manipulated intracellular Ca2+ levels using step-elevations and Ca2+ buffers.
Main Results:
- Photolytic release of cADPr induced a slow Ca2+ release with a delay of several hundred milliseconds.
- In contrast, caged inositol 1,4,5-trisphosphate caused immediate and faster Ca2+ release.
- The delay in cADPr-induced Ca2+ release was abolished by pre-elevated Ca2+ levels and prolonged by Ca2+ buffers.
Conclusions:
- The slow onset of cADPr-induced Ca2+ release is not due to slow channel gating.
- A rise in intracellular Ca2+ from resting levels is necessary for significant cADPr activity.
- Positive calcium feedback is required for full Ca2+ release mediated by cADPr in sea urchin eggs.
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