Induction of M-phase entry of prophase-blocked mouse oocytes through microinjection of okadaic acid, a specific phosphatase inhibitor

Gavin, Anne‐Claude; Tsukitani, Yasumasa; Schorderet‐Slatkine, Sabine

doi:10.1016/0014-4827(91)90159-r

Cited by 82 publications

(68 citation statements)

References 26 publications

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“…PP1 dephosphorylates DCX specifically on amino acid residues S331 and T334 both in vitro and in vivo (31). Microinjection of PP1-neutralizing antibodies (46) and PP1 inhibitors such as okadaic acid (46,47) blocks mitosis and alters the progression of the cell cycle by accumulating at the nucleus to associate with chromatin during G 2 and M phases (46). Our data showed that DCX overexpression blocked the G 2 -M phase of the cell cycle in glioma cells.…”

Section: Discussionmentioning

confidence: 67%

Ectopic Doublecortin Gene Expression Suppresses the Malignant Phenotype in Glioblastoma Cells

Santra¹,

Zhang²,

Santra³

et al. 2006

Cancer Research

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Doublecortin (DCX) is one of the three genes found from Affymetrix gene chip analysis related to glioma patient survival. Two other genes (e.g., osteonectin and semaphorin 3B) are well characterized as antioncogenic and tumor suppressor genes. However, there is no report about the involvement of DCX in cancer. Here, we show that gene transfer technology into DCX-deficient glioblastoma cell lines, such as A172, U87, U251N, RG2, and 9L, with DCX cDNA significantly suppressed growth of these glioma cells. U87 cells with ectopic expression of DCX exhibit a marked suppression of the transformed phenotype as growth arrested in the G 2 phase of the cell cycle progression, small colony formation in soft agar, and no tumor formation in nude rats. This transformed phenotype can be restored by knocking down DCX expression with DCX small interfering RNA. DCX was highly phosphorylated in glioma cells. Phosphorylation in the glioma cells was greater than in noncancer cells such as mouse NIH 3T3 and human embryonic kidney 293T cells. Coimmunoprecipitation of the phosphorylated DCX and spinophilin/neurabin II from DCX-synthesizing glioma cells indicated their interaction. This interaction would lead to a block of anchorage-independent growth as neurabin II is a synergistic inhibitor of anchorage-independent growth with p14ARF (ARF). Interaction between phosphorylated DCX and neurabin II may induce the association of the protein phosphatase 1 catalytic subunit (PP1) with neurabin II and inactivate PP1 and block mitosis during G 2 and M phases of the cell cycle progression. Thus, DCX seems to be a tumor suppressor of glioma. (Cancer Res 2006; 66(24): 11726-35)

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Section: Discussionmentioning

confidence: 67%

Ectopic Doublecortin Gene Expression Suppresses the Malignant Phenotype in Glioblastoma Cells

Santra¹,

Zhang²,

Santra³

et al. 2006

Cancer Research

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“…PP1 mutations in Drosophila (50), yeast (51), and fungi (52) displayed varied mitotic defects and different degrees of lethality. Mitotic blocks were observed upon microinjection of PP1-neutralizing antibodies (53) and PP1 inhibitors such as okadaic acid (54,55). In addition to this, the distribution of PP1 changes with progression of the cell cycle, accumulating at the nucleus to associate with chromatin during G 2 and M phase (53).…”

Section: Discussionmentioning

confidence: 99%

The Human Tumor Suppressor ARF Interacts with Spinophilin/Neurabin II, a Type 1 Protein-phosphatase-binding Protein

Vivo¹,

Calogero²,

Sansone³

et al. 2001

Journal of Biological Chemistry

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The INK4a gene, one of the most often disrupted loci in human cancer, encodes two unrelated proteins, p16INK4a and p14 ARF (ARF) both capable of inducing cell cycle arrest. Although it has been clearly demonstrated that ARF inhibits cell cycle via p53 stabilization, very little is known about the involvement of ARF in other cell cycle regulatory pathways, as well as on the mechanisms responsible for activating ARF following oncoproliferative stimuli. In search of factors that might associate with ARF to control its activity or its specificity, we performed a yeast two-hybrid screen. We report here that the human homologue of spinophilin/neurabin II, a regulatory subunit of protein phosphatase 1 catalytic subunit specifically interacts with ARF, both in yeast and in mammalian cells. We also show that ectopic expression of spinophilin/neurabin II inhibits the formation of G418-resistant colonies when transfected into human and mouse cell lines, regardless of p53 and ARF status. Moreover, spinophilin/ARF coexpression in Saos-2 cells, where ARF ectopic expression is ineffective, somehow results in a synergic effect. These data demonstrate a role for spinophilin in cell growth and suggest that ARF and spinophilin could act in partially overlapping pathways.

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“…Most likely, the lack of a detectable signal resulted from the high level of decondensation of the chromatin in GV oocytes. To overcome this problem, we first cultured the GV oocytes for 24 hours in M2 supplemented with okadaic acid (2.5 FM, Sigma) which induces the condensation of chromatin in GV oocytes including growing ones which are incompetent to resume meiotic maturation (ALEXANDRE et al 1991;GAVIN et al 1991;POLANSKI 1997). After culture the oocytes were fixed using the TARKOWSKI technique (1966) and stained as described above.…”

Section: Immunofluorescencementioning

confidence: 99%

DNA Methylation, Histone Modifications and Behaviour of AKAP95 during Mouse Oocyte Growth and Upon Nuclear Transfer of Foreign Chromatin into Fully Grown Prophase Oocytes

Hoffmann¹,

Tomasik²,

Polanski³

2012

folia biol (krakow)

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HOFFMANN S., TOMASIK G., POLANSKI Z. 2012. DNA methylation, histone modifications and behaviour of AKAP95 during mouse oocyte growth and upon nuclear transfer of foreign chromatin into fully grown prophase oocytes. Folia Biologica (Kraków) 60: [163][164][165][166][167][168][169][170].The poor efficiency of mammalian cloning is due to inappropriate/incomplete epigenetic reprogramming of the donor chromatin. As the success in reprogramming of the donor nucleus may require activity of similar mechanisms which reprogram the chromatin in the course of gametogenesis, we decided to follow the status of some epigenetic markers in the late phase of oogenesis in mice, i.e. in prophase oocytes during their growth and after completion of the growth phase. Our analysis reveals an increase in the level of global DNA methylation starting in oocytes with diameters around 60Fm which was further elevated until completion of oocyte growth. A similar increase was observed in respect to the acetylation of histone H4. On the other hand, the methylation of histone H4 Arg3 was constantly high until the end of oocyte growth, although it differed between fully grown oocytes depending on the type of spatial chromatin organization. We have also studied the AKAP95 protein which was abundant at earlier stages but decreased in fully grown oocytes according to changes in their chromatin organization. The nuclear transfer of different types of donor nuclei with hypomethylated DNA into fully grown prophase oocytes did not increase the global level of methylation of transferred foreign chromatin, regardless if the recipient oocyte was devoid of its own nucleus or its nucleus was left intact. This suggests a major problem in the ability of recipient oocytes to modify donor DNA methylation.

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Induction of M-phase entry of prophase-blocked mouse oocytes through microinjection of okadaic acid, a specific phosphatase inhibitor

Cited by 82 publications

References 26 publications

Ectopic Doublecortin Gene Expression Suppresses the Malignant Phenotype in Glioblastoma Cells

Ectopic Doublecortin Gene Expression Suppresses the Malignant Phenotype in Glioblastoma Cells

The Human Tumor Suppressor ARF Interacts with Spinophilin/Neurabin II, a Type 1 Protein-phosphatase-binding Protein

DNA Methylation, Histone Modifications and Behaviour of AKAP95 during Mouse Oocyte Growth and Upon Nuclear Transfer of Foreign Chromatin into Fully Grown Prophase Oocytes

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