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Role of calcium during release of mollusc oocytes from their blocks in meiotic prophase and metaphase
Author(s) -
Abdelmajid H.,
Guerrier P.,
Colas P.,
Durocher Y.,
Gobet I.,
Krantic S.,
LeclercDavid C.,
Moreau M.,
Néant I.,
Rivailler P.,
Tomkowiak M.
Publication year - 1993
Publication title -
biology of the cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.543
H-Index - 85
eISSN - 1768-322X
pISSN - 0248-4900
DOI - 10.1016/0248-4900(93)90124-w
Subject(s) - prophase , biology , metaphase , meiosis , microbiology and biotechnology , prometaphase , anaphase , mitosis , pronucleus , genetics , zygote , embryo , embryogenesis , chromosome , cell cycle , cell , gene
Summary— Bivalve oocytes constitute an excellent model to study the mechanisms which control cell division, since they arrest at different stages of the meiotic process and respond quite synchronously to various external signals regulating their evolution. Different situations were observed, according to the species, which required a more careful analysis. For example, the same serotonin (5‐HT) signal was found to drive prophase‐arrested oocytes of Spisula to the female pronucleus stage, whereas Ruditapes oocytes stopped in metaphase I. In this last species, 5‐HT treatment thus represents a necessary prerequisite for further development since sperm cannot penetrate prophase‐arrested oocytes, in contrast to the situation found in Spisula . The reasons for these differences cannot be found at the level of the receptors and second messengers. In both species, we found that Ca 2+ was involved as a second messenger and required to release oocytes from their blocks in prophase and metaphase I. This is an unexpected and puzzling situation since MPF is activated by the prophase Ca 2+ surge and inactivated during metaphase‐anaphase transition. The mechanisms underlying these paradoxical situations are discussed, taking into account results from previous observations and experiments. Briefly, our data suggest: I) that the absence of K − sensitive voltage‐gated Ca 2+ channels may be responsible for the unfertilizability of prophasearrested Ruditapes oocytes; and ii) that functional variations in the network of activated kinases present in prophase and metaphase oocytes may be responsible for the divergent responses exhibited by Spisula and Ruditapes oocytes. In particular, these oocytes differ in their sensitivity to Ca 2+ /calmodulin antagonists and in tyrosine phosphorylation of their activated p34 cdc2 kinase.

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