Abstract
Nitric oxide (NO) is identified as a signaling molecule involved in many cellular or physiological functions including meiotic maturation and parthenogenetic activation of mammalian oocytes. We observed that nitric oxide donor SNAP was potent to induce parthenogenetic activation in Xenopus eggs. NO-scavenger CPTIO impaired the effects of SNAP, providing evidence for the effects of the latter to be specific upon NO release. In Xenopus eggs, SNAP treatment induced pigment rearrangement, pronucleus formation and exocytosis of cortical granules. At a biochemical level, SNAP exposure lead to MAPK and Rsk inactivation within 30 minutes whereas MPF remained active, in contrast to calcium ionophore control where MPF activity dropped rapidly. MAPK inactivation could be correlated to pronuclear envelope reformation observed. In SNAP-treated eggs, a strong increase in intracellular calcium level was observed. NO effects were impaired in calcium-free or calcium limited medium, suggesting that that parthenogenetic activation of Xenopus oocytes with a NO donor was mainly calcium-dependent.
Highlights
Nitric oxide (NO) is produced by Nitric Oxide Synthase (NOS) from L-Arginine and molecular oxygen, through a process that can generate L-citruline [1]
Pigment rearrangement were observed in 40% of 2.5 mM SNAP-treated eggs while 77.1% of eggs treated with 5 mM SNAP exhibited pigment rearrangement typical of those observed with control calcium ionophore A23187: the white spot disappeared while pigments were concentrated in the animal hemisphera, moving toward the apex of the cell (Fig. 1B vs 1C)
SNAP induced release of cortical granule lectins in metaphase II-blocked eggs but had no effect on immature oocytes arrested in prophase I since no lectins were detected in the incubating medium (Fig. 1D)
Summary
Nitric oxide (NO) is produced by Nitric Oxide Synthase (NOS) from L-Arginine and molecular oxygen, through a process that can generate L-citruline [1]. Constitutional isoforms of NOS, neuronal NOS (nNOS) and endothelial NOS (eNOS), are calcium and calmodulin-dependent and produce small amounts of NO for a short time lapse [2,3]. An inducible isoform of NOS (iNOS) drives sustained NO production [3,4], which is independent on calcium or calmodulin [5]. NOS have been isolated from a variety of mammalian reproductive tissues like ovary, uterus, testis or epididymis; the role of NO has been emphasized in many physiological processes including reproduction [3,7]. The data collected in the different above-mentioned species suggest that NO might have a widely role in reproduction through mechanisms conserved through evolution but one cannot discard that NO effects may be dependent upon the species considered
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