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Transient reactivation of CSF in parthenogenetic one‐cell mouse embryos
Author(s) -
Ciemerych Maria A,
Kubiak Jacek Z
Publication year - 1999
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 - 10.1111/j.1768-322x.1999.tb01109.x
Subject(s) - maturation promoting factor , biology , interphase , oocyte activation , oocyte , mitosis , microbiology and biotechnology , metaphase , embryonic stem cell , embryo , cell division , kinase , meiosis , cell cycle , cell , biochemistry , cyclin dependent kinase 1 , chromosome , gene
During meiosis, the cytostatic factor (CSF) activity stabilizes the activity of the M‐phase promoting factor (MPF) in metaphase II arrested vertebrate oocytes. Upon oocyte activation, the inactivation of both MPF and CSF enables the entry into the first embryonic mitotic cell cycle. Using a biological assay based on cell‐fusion (hybrid between a parthenogenetically activated egg entering the first mitotic division and an activated oocyte), we observed that in activated mouse oocytes a first drop in CSF activity is detectable as early as 20 min post‐activation. This suggests that CSF is inactivated upon MPF inactivation. However, CSF activity increases again to reach a maximum 60 min post‐activation and gradually disappears during the following 40 min. Thus, in activated mouse oocytes (undergoing the transition to interphase) CSF activity fluctuates before definitive inactivation. We found that hybrids arrested in M‐phase, thus containing CSF activity after oocyte activation, have activated forms of MAP kinases while hybrids in interphase have inactive forms of these enzymes. We postulate that CSF inactivation in mouse oocytes proceeds in two steps. The initial inactivation of CSF, required for MPF inactivation, is transient and does not require MAP kinase inactivation. The final inactivation of CSF, required for normal embryonic cell cycle progression, is dependent upon the inactivation of MAP kinases.