Broad, ectopic expression of the sperm protein PLCZ1 induces parthenogenesis and ovarian tumours in mice

Yoshida, Naoko; Amanai, Manami; Fukui, Tomoyuki; Kajikawa, Eriko; Brahmajosyula, Manjula; Iwahori, Akiko; Nakano, Yoshikazu; Shoji, Shisako; Diebold, Joachim; Hessel, Harald; Huss, Ralf; Perry, Anthony C.F.

doi:10.1242/dev.007930

Cited by 36 publications

(37 citation statements)

References 61 publications

(81 reference statements)

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“…Eight-to 12-week-old B6D2F 1 females were superovulated using standard serial intraperitoneal injections of pregnant mare serum gonadotropin (PMSG) followed 48 hours later by human chorionic gonadotropin (hCG). Oviductal metaphase II (mII) oocytes were collected typically 12 to 15 hours post-hCG injection and cumulus cells removed following hyaluronidase treatment as previously described (Yoshida et al, 2007a).…”

Section: Collection Culture and Activation Of Oocytesmentioning

confidence: 99%

“…Oocytes were cultured for 4 or 7 hours following injection of cRNA or siRNA respectively, and, where appropriate, then transferred to KSOM containing TPEN. i ] within mII oocytes and following 500 M IP 3 injection, ICSI, ethanol treatment, SrCl 2 treatment and/or TPEN treatment was as described previously (Yoshida et al, 2007a). Injection and analysis of mII oocytes was ~18-20 hours after hCG injection.…”

Section: Preparation and Injection Of Crna And Sirnamentioning

confidence: 99%

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Full-term mouse development by abolishing Zn2+-dependent metaphase II arrest without Ca2+ release

Suzuki¹,

Yoshida²,

Suzuki³

et al. 2010

Development

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102

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In vertebrates, a rise in intracellular free Ca2+ (Ca2+i) levels during fertilization initiates second metaphase (mII) exit and the developmental programme. The Ca2+ rise has long been considered to be crucial for development, but verifying this contribution would benefit from defining its role during fertilization. Here, we delineate the role of Ca2+ release during mII exit in wild-type mouse eggs and show that it is dispensable for full-term development. Exit from mII can be induced by Zn2+-specific sequestration without Ca2+ release, eliciting Cyclin B degradation in a manner dependent upon the proteasome pathway and intact microtubules, but not accompanied by degradation of the meiotic regulator Emi2. Parthenogenotes generated by Zn2+ sequestration developed in vitro with normal expression of Ca2+-sensitive genes. Meiotic exit induced by either Ca2+ oscillations or a single Ca2+ rise in oocytes containing a signaling-deficient sperm resulted in comparable developmental rates. In the absence of Ca2+ release, full-term development occurred ∼50% less efficiently, but at readily detectable rates, with the birth of 27 offspring. These results show in intact mouse oocytes that Zn2+ is essential for mII arrest and suggest that triggering meiotic exit is the sole indispensable developmental role of Ca2+ signaling in mammalian fertilization.

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Section: Collection Culture and Activation Of Oocytesmentioning

confidence: 99%

Section: Preparation and Injection Of Crna And Sirnamentioning

confidence: 99%

Full-term mouse development by abolishing Zn2+-dependent metaphase II arrest without Ca2+ release

Suzuki¹,

Yoshida²,

Suzuki³

et al. 2010

Development

Self Cite

102

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“…The actions of PLCζ appears to be specific to egg since transgenic expression of PLCζ in somatic cells appears to have little effect. In the ovary PLCζ expression it leads to spontaneous egg activation and the subsequent development of ovarian teratocarcinomas (Yoshida et al, 2007).…”

Section: Signalling By a Sperm Factormentioning

confidence: 99%

The dynamics of calcium oscillations that activate mammalian eggs

Swann¹,

Yu²

2008

Int. J. Dev. Biol.

121

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It has been known for some time that mammalian eggs are activated by a series of intracellular calcium oscillations that occur shortly after sperm egg membrane fusion. Recent work has identified a novel sperm specific phospholipase C zeta as the likely agent that stimulates the calcium oscillations in eggs after sperm-egg membrane fusion. PLCzeta is stimulated by low intracellular calcium levels in a manner which suggests that there is a regenerative feedback of calcium release and PLCzeta induced inositol 1,4,5-trisphophate (InsP 3 ) production in eggs. This implies calcium oscillations in fertilizing mammalian eggs are driven by underlying oscillations of InsP 3 . This model of oscillations is supported by the response of mouse eggs to sudden increases in InsP 3 . The cellular targets of calcium oscillations include calmodulin-dependent protein kinases, protein kinase C and mitochondria. There is evidence that eggs might be best activated by multiple calcium increases rather than a single calcium rise. As yet we do not fully understand how the target of calcium in a mammalian egg might decode the patterns of calcium changes that can occur during egg activation.

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“…Indeed females that overexpress the sperm protein PLCZ1 in oocytes show normal oocyte meiotic progression, yet induce parthenogenetic activation of their eggs and display even greater rates of teratocarninomas than mos−/− females. 74 Altogether, these results argue that it is mostly parthenogenetic activation and not increase in cortical tension that causes ovarian teratomas.…”

Section: Mouse Oocyte a Paradigm Of Cancer Cellmentioning

confidence: 88%