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Lookup NU author(s): Dr Mark Levasseur
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Fertilisation in ascidians triggers a series of periodic rises in cytosolic Ca2+ that are essential for release from metaphase I arrest and progression through meiosis II. These sperm-triggered Ca2+ oscillations are switched off at exit from meiosis II. Ascidian zygotes provided the first demonstration of the positive feedback loop whereby elevated Cdk1 activity maintained these Ca2+ oscillations. Since then it has been reported that Cdk1 sensitises the type I inositol trisphosphate [Ins(1,4,5)P,3] receptor in somatic cells, and that sperm-triggered Ca2+ oscillations in mouse zygotes stop because the forming pronuclei sequester phospholipase C zeta that was delivered to the egg by the fertilising sperm. Here, using enucleation, we demonstrate in ascidian eggs that Ca2+ spiking stops at the correct time in the absence of pronuclei. Sequestration of sperm factor is therefore not involved in terminating Ca2+ spiking for these eggs. Instead we found that microinjection of the Cdk1 inhibitor p21 blocked Ca2+ spiking induced by ascidian sperm extract (ASE). However, such eggs were still capable of releasing Ca2+ in response to Ins(1,4,5)P3 receptor agonists, indicating that ASE-triggered Ca2+ oscillations can stop even though the response to Ins(14,5)P3 remained elevated. These data suggest that Cdk1 activity promotes Ins(1,4,5)P3 production in the presence of the sperm factor, rather than sensitising the Ca2+ releasing machinery to Ins(1,4,5)P3. These findings suggest a new link between this cell cycle kinase and the Ins(14,5)P3 pathway.
Author(s): Levasseur M, Carroll M, Jones KJ, McDougall A
Publication type: Article
Publication status: Published
Journal: Journal of Cell Science
ISSN (print): 0021-9533
ISSN (electronic): 1477-9137
Publisher: The Company of Biologists Ltd.
PubMed id: 17502483
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