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Nitric oxide-donor SNAP induces Xenopus eggs activation
Michal Jeseta1, Matthieu Marin, Hana Tichovska
1Veterinary Research Institute, Department of Genetics and Reproduction, Brno, Czech Republic. jeseta@vri.cz
Plos One
|August 23, 2012
Summary
Nitric oxide (NO) triggers parthenogenetic activation in Xenopus eggs, initiating key developmental events. This NO-mediated activation is primarily dependent on intracellular calcium release.
Area of Science:
- Cellular biology
- Developmental biology
- Reproductive biology
Background:
- Nitric oxide (NO) is a crucial signaling molecule in mammalian oocyte maturation and activation.
- Understanding NO's role in non-mammalian oocyte activation is essential for comparative developmental studies.
Purpose of the Study:
- To investigate the role of nitric oxide (NO) in the parthenogenetic activation of Xenopus oocytes.
- To elucidate the biochemical mechanisms underlying NO-induced oocyte activation.
Main Methods:
- Treatment of Xenopus eggs with a nitric oxide donor (SNAP) and an NO-scavenger (CPTIO).
- Observation of morphological changes (pigment rearrangement, pronucleus formation, cortical granule exocytosis).
- Biochemical analysis of maturation-promoting factor (MPF), MAPK, and Rsk activity.
- Measurement of intracellular calcium levels and assessment in calcium-depleted media.
Main Results:
- SNAP treatment induced parthenogenetic activation, evidenced by pigment rearrangement, pronucleus formation, and cortical granule exocytosis.
- SNAP exposure led to rapid inactivation of MAPK and Rsk, while MPF remained active, distinct from calcium ionophore effects.
- SNAP induced a significant increase in intracellular calcium, and its effects were diminished in calcium-free conditions.
Conclusions:
- Nitric oxide (NO) can induce parthenogenetic activation in Xenopus oocytes.
- NO-mediated activation involves the regulation of MAPK and Rsk pathways.
- The parthenogenetic activation of Xenopus oocytes by NO donors is largely dependent on intracellular calcium.

