Cdc25b phosphatase is required for resumption of meiosis during oocyte maturation

Lincoln, A. Jeannine; Wickramasinghe, Dineli; Stein, Paula; Schultz, Richard M.; Palko, Mary Ellen; Miguel, Maria De De P.; Tessarollo, Lino; Donovan, Peter

doi:10.1038/ng856

Cited by 261 publications

(203 citation statements)

References 24 publications

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“…This suggests that they have distinct biological functions in embryonic and adult mice. Mice lacking CDC25B and CDC25C, individually or in combination, are viable and develop normally, and embryonic fibroblasts derived from these mice exhibit normal cell cycle parameters in culture (11)(12)(13). These findings demonstrate that mice can survive throughout embryogenesis and adulthood with a single member of the family, CDC25A.…”

mentioning

confidence: 72%

Response of small intestinal epithelial cells to acute disruption of cell division through CDC25 deletion

Lee¹,

White

Hurov

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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The CDC25 protein phosphatases (CDC25A, B, and C) drive cell cycle transitions by activating key components of the cell cycle engine. CDC25A and CDC25B are frequently overproduced in human cancers. Disruption of Cdc25B or Cdc25C individually or in combination has no effect on mouse viability. Here we report that CDC25A is the only family member to provide an essential function during early embryonic development, and that other family members compensate for its loss in adult mice. In contrast, conditional disruption of the entire family is lethal in adults due to a loss of small intestinal epithelial cell proliferation in crypts of Lieberkü hn. Cdc25 loss induced Wnt signaling, and overall crypt structures were preserved. In the face of continuous Wnt signaling, nearly all crypt epithelial progenitors differentiated into multiple cell lineages, including crypt base columnar cells, a proposed stem cell. A small population of Musashi/Dcamkl-1/nuclear ␤-catenin-positive epithelial cells was retained in these crypts. These findings have implications for the development of novel, less cytotoxic cancer chemotherapeutic drugs that specifically target the cell cycle.CDC25 phosphatases ͉ cell cycle ͉ stem cells T he CDC25 phosphatases promote cell cycle progression by activating cyclin-dependent protein kinases (1-6). In mice, Cdc25A, B, and C exhibit overlapping but distinct patterns of expression during development and in adult tissues (7-10). This suggests that they have distinct biological functions in embryonic and adult mice. Mice lacking CDC25B and CDC25C, individually or in combination, are viable and develop normally, and embryonic fibroblasts derived from these mice exhibit normal cell cycle parameters in culture (11-13). These findings demonstrate that mice can survive throughout embryogenesis and adulthood with a single member of the family, CDC25A. Here we report the consequences of deleting Cdc25A alone and in combination with Cdc25B and Cdc25C in mice. Our data demonstrate that CDC25A provides an essential function during early embryogenesis, and that CDC25B and/or CDC25C compensate for CDC25A loss in adult mice. In contrast, mice lacking all 3 CDC25s die within 1 week due to complete loss of epithelial cell proliferation in the small intestinal crypts.We used this model to explore how small intestine stem and progenitor cells respond to the acute disruption of cell division. The self-renewing epithelium of the adult small intestine contains tetrapotent stem cells that give rise to rapidly proliferating committed daughter cells, which in turn produce terminally differentiated cells (14). One of these lineages, Paneth cells, are located in crypts of Lieberkühn along with stem and progenitor cells. Analysis of gene expression and cellular morphology, as well as lineage tracing experiments, suggest that stem cells are intermingled with or lie just above Paneth cells at the crypt base (15-18). These stem cells are considered to provide the source of recovery after damage to the epithelial lining from such facto...

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mentioning

confidence: 72%

Response of small intestinal epithelial cells to acute disruption of cell division through CDC25 deletion

Lee¹,

White

Hurov

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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“…However, contrary to Plk1, interference with the function of Cdc25B does not appear to have a major impact on cell cycle progression in unperturbed cells (van Vugt et al, 2004a). This is further supported by the finding that mice lacking functional Cdc25B are viable and healthy (Lincoln et al, 2002). Therefore, inhibition of Cdc25B appears to be an attractive target for combinational therapy without running the risk of provoking tumor onset through genetic instability.…”

Section: Plk1 and Cancermentioning

confidence: 90%

“…However, Cdc25B was shown to be activated by Cyclin A-Cdk2 and Cyclin A-Cdk2 activity is present from S phase onwards (Gabrielli et al, 1997). Moreover, deletion of the Cdc25B gene does not block somatic cell division, so additional levels of regulation must exist (Lincoln et al, 2002). Interestingly, more and more evidence is accumulating that the (maturing) centrosome could play a key role in the initial activation of Cyclin B-Cdk1.…”

Section: Plk1 and Mitotic Entrymentioning

confidence: 99%

Getting in and out of mitosis with Polo-like kinase-1

2005

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“…Oocytes from cdc25b Ϫ/Ϫ mice are unable to resume meiosis and remain arrested in prophase unless rescued by microinjection of Cdc25B mRNA. Cdc25A and Cdc25C, although present in the oocyte, did not compensate for this function (Lincoln et al, 2002). Conversely, cdc25c Ϫ/Ϫ females are fertile, suggesting its distinct function (Chen et al, 2001).…”

Section: Introductionmentioning

confidence: 91%

Protein kinase a modulates Cdc25B activity during meiotic resumption of mouse oocytes

Zhang

et al. 2008

Developmental Dynamics

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Protein kinase A (PKA) play a critical role in maintaining the meiotic arrest. However, the steps downstream of PKA remain largely unknown. In this study, we investigated the regulation of meiotic resumption by PKA/Cdc25B pathway in mouse oocytes. Injection of mRNA coding for Cdc25b-S321A had a more potent maturation-inducing ability than Cdc25b-WT. When co-injected with PKA inhibitor, Cdc25B-WT had similar activities with Cdc25B-S321A. Meanwhile, the phosphorylation of Cdc25B-S321 was detected in germinal vesicle (GV) oocytes by Western blotting with a phospho-Ser321-specific antibody and the band disappeared when oocytes reenter into the meiotic cell cycle. Furthermore, Cdc25B-WT translocated to the nucleus shortly before GV breakdown (GVBD), whereas phosphorylated Cdc25B-S321 expressed exclusively in the cytoplasm and the signal could not be detected in GVBD oocytes. Taken together, these data indicate that Cdc25B-Serine321 is the potential PKA target and Cdc25B subcellular localization determines its function during the process of maintaining GV arrest in mouse oocytes. Developmental Dynamics 237: 3777-3786, 2008.

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Cdc25b phosphatase is required for resumption of meiosis during oocyte maturation

Cited by 261 publications

References 24 publications

Response of small intestinal epithelial cells to acute disruption of cell division through CDC25 deletion

Response of small intestinal epithelial cells to acute disruption of cell division through CDC25 deletion

Getting in and out of mitosis with Polo-like kinase-1

Protein kinase a modulates Cdc25B activity during meiotic resumption of mouse oocytes

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