Parthenogenetic activation of oocytes in c-mos-deficient mice

Hashimoto, Naohiro; Watanabe, Nobumoto; Furuta, Yasuhide; Tamemoto, Hiroyuki; Sagata, Noriyuki; Yokoyama, Minesuke; Okazaki, Kenji; Nagayoshi, Mariko; Takeda, Nobuo; Ikawa, Yoji; Aizawa, Shinichi

doi:10.1038/370068a0

Cited by 415 publications

(284 citation statements)

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“…The Mos pathway in mouse, however, does not precisely parallel that in Xenopus. Oocytes from Mos knockout mice arrest properly at metaphase of meiosis II (Hashimoto et al, 1994), but then spontaneously exit meiosis after 2-4 hr (Verlhac et al, 1996;Colledge et al, 2004). Therefore, Mos is necessary to maintain, but not establish, meiotic arrest in mouse.…”

Section: Meiosis Arrest and Release In Vertebratesmentioning

confidence: 99%

Transitioning from egg to embryo: Triggers and mechanisms of egg activation

Horner

Wolfner

2008

Developmental Dynamics

181

177

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The transition from mature oocyte to developing embryo requires a coordinated series of events, collectively known as egg activation. Egg activation includes changes to egg coverings to prevent polyspermy, release of oocyte meiotic arrest, generation of haploid female and male pronuclei, changes in maternal mRNAs and protein populations, and cytoskeletal rearrangements. In many animals, egg activation is triggered by fertilization, which increases intracellular calcium within the oocyte and thereby regulates molecular events of egg activation. In other animals, fertilization-independent external signals, including mechanical stimulation of eggs and/or changes in ionic milieu, trigger activation. Recent studies have clarified the upstream portion of pathways leading to eggshell changes and cell cycle resumption and have identified activation-induced changes in maternal mRNA and protein profiles that can identify molecular players in the downstream events of egg activation. We review signals that trigger activation and how they link to subsequent molecular events of egg activation. Developmental Dynamics 237:527-544, 2008.

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Section: Meiosis Arrest and Release In Vertebratesmentioning

confidence: 99%

Transitioning from egg to embryo: Triggers and mechanisms of egg activation

Horner

Wolfner

2008

Developmental Dynamics

181

177

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“…Our previous study [11] showed that MAP kinase might be involved in microtubule nucleation by -tubulin in pig oocytes. However, it was reported that mouse oocytes deficient in MAP kinase activity could still divide and release polar bodies [6,[12][13][14]. Until now, the targets of MAP kinase in the meiotic spindle remain unclear.…”

Section: Introductionmentioning

confidence: 99%

“…It is well established that the MII arrest is maintained by cytostatic factor (CSF) activity, with MOS/MEK/ERK cascade being its essential components [4,10,12,13,15]. Although existing evidence has suggested that MAP kinase is important for metaphase arrest, almost all data come from mos -/-oocytes or other models indication MAP kinase is not activated during the entire maturation process.…”

Section: Introductionmentioning

confidence: 99%

Effects of MEK inhibitor U0126 on meiotic progression in mouse oocytes: microtuble organization, asymmetric division and metaphase II arrest

et al. 2003

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In this study we used U0126, a potent and specific inhibitor of MEK, to study the roles of MEK/ERK/p90 rsk signaling pathway in the meiotic cell cycle of mouse oocytes. The phosphorylation of MAP kinase and p90 rsk in the oocytes treated with 1.5 M U0126 was the same as that in oocytes cultured in drug-free medium. With 1.5 M U0126 treatment, the spindles appeared normal as they formed in oocytes, but failed to maintain its structure. Instead, the spindle lost one pole or elongated extraordinarily. After further culture, some oocytes extruded gigantic polar bodies (>30 m) that later divided into two small ones. Some oocytes underwent symmetric division and produced two equal-size daughter cells in which normal spindles formed. In oocytes with different division patterns, MAP kinase was normally phosphorylated. When the concentration of U0126 was increased to 15 M, the phosphorylation of both MAPK and p90 rsk were inhibited, while symmetric division was decreased. When incubating in medium containing 15 M U0126 for 14 h, oocytes were activated, but part of them failed to emit polar bodies. MII oocytes were also activated by 15 M U0126, at the same time the dephosphorylation of MAP kinase and p90 rsk was observed. Our results indicate that 1) MEK plays important but not indispensable roles in microtubule organization; 2) MEK keeps normal meiotic spindle morphology, targets peripheral spindle positioning and regulates asymmetric division by activating some unknown substrates other than MAP kinase /p90 rsk ; and 3) activation of MEK/ERK/p90 rsk cascade maintains MII arrest in mouse oocytes.

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“…In mos-deficient mice or in mouse oocytes injected with mos double-stranded RNA, approximately 60 -75% of oocytes fail to arrest at metaphase II and undergo parthenogenetic activation (Choi et al, 1996;Colledge et al, 1994;Hashimoto et al, 1994;Wianny and Zernicka-Goetz, 2000). In this study, microinjection of 340 pg of mos MO, 17 pg of mos MO, or 340 pg of control MO into the cytoplasm of germinal vesicle stage mouse oocytes resulted in respective parthenogenetic activation rates of 56, 23, and 0% when scored 20 h after 3-isobutyl-1-methyl-xanthine (IBMX) removal (Fig.…”

mentioning

confidence: 99%