Ser 15 of WEE1B is a potential PKA phosphorylation target in G2/M transition in one-cell stage mouse embryos

Liu, Chao; Liu, Yang; Wu, Dongcheng; Luan, Zhidong; Wang, Enhua; Yu, Bin

doi:10.3892/mmr.2013.1437

Cited by 10 publications

(6 citation statements)

References 48 publications

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“…75 WEE2 has been shown to be involved in G2/M transition of one-cell-stage mouse embryos. 76 Interestingly, WEE2 mRNA was found to be exclusively expressed in mouse MII oocytes and to abruptly decrease after fertilization, 77 while our data showed WEE2 protein to become 1.7-fold more abundant until the 4-cell stage, demonstrating the disparity between transcript and protein abundance during embryogenesis.…”

Section: Protein Abundance Profiles Of Key Players In Mitosis and Meicontrasting

confidence: 64%

Stage-Specific Proteome Signatures in Early Bovine Embryo Development

et al. 2014

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Development of early embryonic stages before activation of the embryonic genome depends on sufficiently stored products of the maternal genome, adequate recruitment and degradation of mRNAs, as well as activation, deactivation, and relocation of proteins. By application of an isobaric tagging for relative and absolute quantification (iTRAQ)-based approach, the proteomes of bovine embryos at the zygote and 2-cell and 4-cell stage with MII oocytes as a reference were quantitatively analyzed. Of 1072 quantified proteins, 87 differed significantly in abundance between the four stages. The proteomes of 2-cell and 4-cell embryos differed most from the reference MII oocyte, and a considerable fraction of proteins continuously increased in abundance during the stages analyzed, despite a strongly attenuated rate of translation reported for this period. Bioinformatic analysis revealed particularly interesting proteins involved in the p53 pathway, lipid metabolism, and mitosis. Verification of iTRAQ results by targeted SRM (selected reaction monitoring) analysis revealed excellent agreement for all five proteins analyzed. By principal component analysis, SRM quantifications comprising a panel of only five proteins were shown to discriminate between all four developmental stages analyzed here. For future experiments, an expanded SRM protein panel will provide the potential to detect developmental disturbances with high sensitivity and enable first insights into the underlying molecular pathways.

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Section: Protein Abundance Profiles Of Key Players In Mitosis and Meicontrasting

confidence: 64%

Stage-Specific Proteome Signatures in Early Bovine Embryo Development

et al. 2014

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“…Microinjection of Cdc25b -S321A mRNA or Cdc25b -WT mRNA solely served as the positive controls. Our recent study demonstrated WEE1B is a potential PKA target and Ser 15 phosphorylation of WEE1B is required for PKA-induced MPF inhibition in fertilized mouse eggs [30]. Since WEE1B may be phosphorylated by exogenous dbcAMP, we also detected the expression levels of various Cdc25b and 14-3-3ε mRNAs in eggs with WEE1B-Ser 15 phosphorylation.…”

Section: Resultsmentioning

confidence: 99%

14-3-3 epsilon prevents G2/M transition of fertilized mouse eggs by binding with CDC25B

et al. 2014

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BackgroundThe 14-3-3 (YWHA) proteins are highly conserved in higher eukaryotes, participate in various cellular signaling pathways including cell cycle regulation, development and growth. Our previous studies demonstrated that 14-3-3ε (YWHAE) is responsible for maintaining prophase | arrest in mouse oocyte. However, roles of 14-3-3ε in the mitosis of fertilized mouse eggs have remained unclear. Here, we showed that 14-3-3ε interacts and cooperates with CDC25B phosphorylated at Ser321 regulating G2/M transition of mitotic progress of fertilized mouse eggs.ResultsDisruption of 14-3-3ε expression by RNAi prevented normal G2/M transition by inhibition of MPF activity and leaded to the translocation of CDC25B into the nucleus from the cytoplasm. Overexpression of 14-3-3ε-WT and unphosphorylatable CDC25B mutant (CDC25B-S321A) induced mitotic resumption in dbcAMP-arrested eggs. In addition, we examined endogenous and exogenous distribution of 14-3-3ε and CDC25B. Endogenous 14-3-3ε and CDC25B were co-localized primarily in the cytoplasm at the G1, S, early G2 and M phases whereas CDC25B was found to accumulate in the nucleus at the late G2 phase. Upon coexpression with RFP–14-3-3ε, GFP–CDC25B–WT and GFP–CDC25B–S321A were predominantly cytoplasmic at early G2 phase and then GFP–CDC25B–S321A moved to the nucleus whereas CDC25B-WT signals were observed in the cytoplasm without nucleus accumulation at late G2 phase at presence of dbcAMP.ConclusionsOur data indicate that 14-3-3ε is required for the mitotic entry in the fertilized mouse eggs. 14-3-3ε is primarily responsible for sequestering the CDC25B in cytoplasm and 14-3-3ε binding to CDC25B-S321 phosphorylated by PKA induces mitotic arrest at one-cell stage by inactivation of MPF in fertilized mouse eggs.

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“…For example, Ube2c encodes a ubiquitin-conjugating enzyme known to regulate mitotic exit by promoting cyclin B degradation (Ben-Eliezer et al, 2015;Hao et al, 2012). Moreover, overexpression of the kinase Wee1 might delay cell cycle progression in oocytes and early embryos that is normally controlled by Wee1b and/or Wee2 (Han et al, 2005;Liu et al, 2013).…”

Section: Setdb1 Controls Gene Expression During Oogenesismentioning

confidence: 99%

The methyltransferase Setdb1 is essential for meiosis and mitosis in mouse oocytes and early embryos

et al. 2016

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Oocytes develop the competence for meiosis and early embryogenesis during their growth. Setdb1 is a histone H3 lysine 9 (H3K9) methyltransferase required for post-implantation development and has been implicated in the transcriptional silencing of genes and endogenous retroviral elements (ERVs). To address its role in oogenesis and pre-implantation development, we conditionally deleted Setdb1 in growing oocytes. Loss of Setdb1 expression greatly impaired meiosis. It delayed meiotic resumption, altered the dynamics of chromatin condensation, and impaired kinetochore-spindle interactions, bipolar spindle organization and chromosome segregation in more mature oocytes. The observed phenotypes related to changes in abundance of specific transcripts in mutant oocytes. Setdb1 maternally deficient embryos arrested during pre-implantation development and showed comparable defects during cell cycle progression and in chromosome segregation. Finally, transcriptional profiling data indicate that Setdb1 downregulates rather than silences expression of ERVK and ERVLMaLR retrotransposons and associated chimearic transcripts during oogenesis. Our results identify Setdb1 as a newly discovered meiotic and embryonic competence factor safeguarding genome integrity at the onset of life.

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Ser 15 of WEE1B is a potential PKA phosphorylation target in G2/M transition in one-cell stage mouse embryos

Cited by 10 publications

References 48 publications

Stage-Specific Proteome Signatures in Early Bovine Embryo Development

Stage-Specific Proteome Signatures in Early Bovine Embryo Development

14-3-3 epsilon prevents G2/M transition of fertilized mouse eggs by binding with CDC25B

The methyltransferase Setdb1 is essential for meiosis and mitosis in mouse oocytes and early embryos

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