MAP kinase cascade, but not ERKs, activated during early cleavage of mouse embryos

Haraguchi, Satoru; Naito, Kunihiko; Sato, Eimei

doi:10.1002/(sici)1098-2795(199810)51:2<148::aid-mrd4>3.0.co;2-q

Cited by 17 publications

(11 citation statements)

References 46 publications

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“…Bovine preimplantation embryos treated alone with UO126 did not display an impaired ability to develop to the blastocyst stage. This result is in accordance with outcomes from similar experiments applied to the mouse embryo, suggesting that the ERK pathway is not required to sustain development to the blastocyst stage (Haraguchi et al 1998, Natale et al 2004. When both inhibitors are combined, we observed an unexpected outcome.…”

Section: Discussioncontrasting

confidence: 99%

“…It can be concluded that ERK protein was localized in the cytoplasm and the nucleus, suggesting that the ERK pathway is also active in bovine embryos. This finding is different from that in mouse where there are conflicting reports about the role of ERK in preimplantation embryogenesis (Haraguchi et al 1998, Iwamori et al 2000, Wang et al 2004. It has been suggested that ERK is not phosphorylated at any stage during the cell cycle of the mouse early embryos (Iwamori et al 2000); although ERK proteins are expressed, MAPKs other than ERKs are activated during the early cleavage divisions of mouse embryos (Haraguchi et al 1998).…”

Section: Discussionsupporting

confidence: 94%

“…This finding is different from that in mouse where there are conflicting reports about the role of ERK in preimplantation embryogenesis (Haraguchi et al 1998, Iwamori et al 2000, Wang et al 2004. It has been suggested that ERK is not phosphorylated at any stage during the cell cycle of the mouse early embryos (Iwamori et al 2000); although ERK proteins are expressed, MAPKs other than ERKs are activated during the early cleavage divisions of mouse embryos (Haraguchi et al 1998). However, recently it has been reported that ERK1/2 mRNA could be detected from the oocyte to the blastocyst stage in the mouse embryo and, in addition, ERK1/2 proteins are activated by phosphorylation (Wang et al 2004).…”

Section: Discussionmentioning

confidence: 99%

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Mitogen-activated protein kinase (MAPK) blockade of bovine preimplantation embryogenesis requires inhibition of both p38 and extracellular signal-regulated kinase (ERK) pathways

Madan¹,

Calder²,

Watson³

2005

Reproduction

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Blastocyst formation, as a critical period during development, is an effective indicator of embryonic health and reproductive efficiency. Out of a number of mechanisms underlying blastocyst formation, highly conserved mitogen-activated protein kinase (MAPK) signaling has emerged as a major mechanism involved in regulating murine preimplantation embryo development. The objective of our study was to ascertain the role of MAPK signaling in regulating bovine development to the blastocyst stage. Using reverse transcriptase PCR and immunohistochemical staining procedures we have demonstrated that mRNA transcripts and polypeptides encoding p38 MAPK pathway constituents are detectable in preimplantation bovine embryos from the one-cell to the blastocyst stage. Further, the effects on bovine embryo development following inhibition of p38a/b and extracellular signal-regulated kinase (ERK) signaling by treatment with SB220025 and U0126, respectively, were investigated. Eight-cell bovine embryos (50 per group; three replicates) were placed into treatments consisting of synthetic oviductal fluid (SOF) medium: SOF 1 SB202474 (inactive analogue), SOF 1 SB220025, SOF 1 U0124 (inactive analogue), SOF 1 U0126, and SOF 1 SB220025 1 U0126. Inhibition of p38 MAPK or ERK signaling individually did not affect development to the blastocyst stage. However, when both pathways were blocked simultaneously there was a significant reduction (P < 0.05) in blastocyst formation, cell number and immunofluorescence of phosphorylated downstream pathway constituents. We have determined that, in variance to what was observed during murine preimplantation development, bovine early embryos progress at normal frequencies to the blastocyst stage in the presence of p38 MAPK inhibitors.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 99%

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Mitogen-activated protein kinase (MAPK) blockade of bovine preimplantation embryogenesis requires inhibition of both p38 and extracellular signal-regulated kinase (ERK) pathways

Madan¹,

Calder²,

Watson³

2005

Reproduction

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“…The embryos without EGFP illumination were omitted from further analyses. Phosphorylated forms of ERK1 and 2, major MAPKs in mouse oocytes, and hyperphosphorylated forms of RSK were detected in MII oocytes, but not in developing embryos as reported previously [20,21]. In contrast, clear phosphorylation was observed at both 24 and 48 h of culture in embryos injected with the SDSE-MEK expression vector (Fig.…”

Section: The Effects Of Sdse-mek Expression On the Mapk/ Rsk States Asupporting

confidence: 53%

Mos and the Mitogen-Activated Protein Kinase Do Not Show Cytostatic Factor Activity in Early Mouse Embryos

Kashima

Kanô

Naito

2007

Journal of Reproduction and Development

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Abstract. Mos and the mitogen-activated protein kinase (MAPK) cascade have been established as crucial regulators of second meiotic metaphase arrest, the so-called CSF arrest, in mammalian oocytes. They are also thought to play a role in regulating mitotic metaphase arrest of early mammalian embryos. In the present study, we examined whether mitotic arrest is induced in early mouse embryos by activation of extracellular signal-regulated kinases (ERKs), which are major MAPKs in mouse eggs, and their substrate, p90Ribosomal S6 kinase (RSK), as reported in Xenopus embryos. Wild-type Mos (wt-Mos), degradation-resistant Mos mutant (P2G-Mos) or constitutive active mutant of MAPK/ERK kinase, MEK (SDSE-MEK), was expressed in early mouse embryos by injecting the respective expression vectors into the pronucleus of fertilized eggs, and the developmental rates were then examined up to 72 h after insemination. Expression of P2G-Mos and SDSE-MEK succeeded in activating ERKs and RSK in developing mouse embryos, while wt-Mos failed to activate them in spite of expression of mos mRNA, indicating that the wt-Mos protein is unstable in early mouse embryos. Although the activated levels of ERKs and RSK in the vector-injected embryos were comparable to those of meiotically arrested mouse oocytes, their developmental rates were identical to those of the control embryos. These results suggest that activation of MAPK and RSK does not induce mitotic arrest in early mouse embryos. The present study indicates that there are large physiological differences between early mouse embryos and mouse oocytes and that CSF arrest of mouse eggs in mitosis should be discussed separately from that in meiosis. Key words: Cell cycle, Cytostatic factor (CSF), MEK, Metaphase arrest, Mouse, p90Ribosomal S6 kinase (RSK) (J. Reprod. Dev. 53: [1175][1176][1177][1178][1179][1180][1181][1182] 2007) nfertilized vertebrate oocytes arrest their meiosis in the second meiotic metaphase (MII), resume meiosis in response to a fertilization stimulus and proceed to early development. In developing frog embryos, metaphase arrest has been induced by injection of MII oocyte cytoplasm, and this indicates that the frog MII oocyte contains cytostatic factor (CSF), which arrests the cell cycle at metaphase not only in meiotic oocytes but also in mitotic embryos [1]. Many studies on CSF have been conducted in Xenopus, and Mos, an oocytespecific mitogen-activated protein kinase (MAPK) kinase kinase, has been shown to play crucial roles in CSF activity. Injection of mos mRNA or Mos protein into 2-cell embryos induces mitotic arrest, and removal of Mos from MII oocyte cytoplasm results in loss of this activity [2,3]. The same activity has been reported in constitutive active MAPK and Raf-1, a MAPK cascade activator, indicating that this CSF activity of Mos is mediated by the MAPK cascade [3,4]. In addition, mediation of CSF activity by p90Ribosomal S6 kinase (RSK), a substrate of

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“…However, MAP kinase activity can be also assayed by its ability to phosphorylate MBP (myelin basic protein) in an in vitro assay. Importantly, during the first but not the second mitosis an MBP activity was detectable in such assay suggesting the possible activity of other MAP kinase(s) (Verlhac et al, 1994;Haraguchi et al, 1998). p90 rsk1…”

Section: First Embryonic Mitosis: Meiosis-like Mitosis or How And Whmentioning

confidence: 99%

On the transition from the meiotic to mitotic cell cycle during early mouse development

Kubiak

Ciemerych²,

Hupalowska³

et al. 2008

Int. J. Dev. Biol.

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Here, we outline the mechanisms involved in the regulation of cell divisions during oocyte maturation and early cleavages of the mouse embryo. Our interest is focused on the regulation of meiotic M-phases and the first embryonic mitoses that are differently tuned and are characterized by specifically modified mechanisms, some of which have been recently identified. The transitions between the M-phases during this period of development, as well as associated changes in their regulation, are of key importance for both the meiotic maturation of oocytes and the further development of the mammalian embryo. The mouse is an excellent model for studies of the cell cycle during oogenesis and early development. Nevertheless, a number of molecular mechanisms described here were discovered or confirmed during the study of other species and apply also to other mammals including humans. KEY WORDS: meiosis, mitosis, oocyte, embryo, MPF, CSF, spindle assembly checkpoint, Mad2, Rec8Cell cycle is often modified in different cell types during development and aging of the individual. These adaptations seem to be of a particular importance for the success of the early developmental program. The cell cycle must be modified during meiosis, when DNA replication is suppressed, during spermatogenesis in males and in oocytes undergoing the process of meiotic maturation in females. The oocyte enters the first meiotic prophase that can take several years. Then, in sexually mature females, the oocyte resumes meiosis and progress through two M-phases of the meiotic maturation, each of them differently regulated, to assure correct separation of maternal chromatin. Fertilized egg transits from meiotic to the mitotic cell cycle and resume DNA replication.In the current review we will focus on M-phase modifications that are the subject of the research in our laboratories. We choose three examples of specific M-phase adjustments i.e. metaphase I, and metaphase II of oocyte meiotic divisions and the first mitosis of mouse embryo. We center our attention on the temporal regulation of metaphase I progression and the singularities of the spindle assembly checkpoint during this period, mechanisms of sustaining and exiting metaphase II-arrest, and finally the unique regulation of the first embryonic mitosis. The correct timing of Int.

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MAP kinase cascade, but not ERKs, activated during early cleavage of mouse embryos

Cited by 17 publications

References 46 publications

Mitogen-activated protein kinase (MAPK) blockade of bovine preimplantation embryogenesis requires inhibition of both p38 and extracellular signal-regulated kinase (ERK) pathways

Mitogen-activated protein kinase (MAPK) blockade of bovine preimplantation embryogenesis requires inhibition of both p38 and extracellular signal-regulated kinase (ERK) pathways

Mos and the Mitogen-Activated Protein Kinase Do Not Show Cytostatic Factor Activity in Early Mouse Embryos

On the transition from the meiotic to mitotic cell cycle during early mouse development

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