Parthenogenetic development ofMos-deficient mouse oocytes

Abstract

Ovarian teratomas develop in Mos−/− mutant mice produced by homologous recombination. These teratomas are probably derived from oocytes that undergo spontaneous parthenogenetic activation within the ovaries. However, it is not clear how the activated eggs develop into teratomas since embryonic development beyond the four‐cell stage was not observed either in vitro or in vivo. In this study, Mos−/− parthenotes derived from in vitro‐matured oocytes were cultured using a recently developed medium, KSOM/AA, which promotes a high frequency of preimplantation development by normal embryos. In total, 5% of the Mos−/− oocytes developed to the blastocyst stage. Preimplantation‐like and early postimplantation‐like embryos were observed in the ovaries of 60–63‐day‐old Mos−/− mice. These observations support the hypothesis that Mos−/− teratomas are derived from parthenogenetically activated oocytes that undergo early embryonic development up to early postimplantation‐like stages within the ovaries. Aberrant meiotic divisions commonly observed in Mos−/− oocytes in vitro may adversely affect preimplantation development and reduce the frequency of blastocyst formation even under the best culture conditions. Mol. Reprod. Dev. 48:391–396, 1997. © 1997 Wiley‐Liss, Inc.

A rare germline BMP15 missense mutation causes hereditary ovarian immature teratoma in human

“…3 B ) and the appearance of two-cell structures ( Fig. 3 C ) were considered to indicate parthenogenesis ( 23 ). We observed that the proportion of parthenogenetic activation was 8.4% in mice with the CC genotype, 32.5% in mice with the CT genotype, and 51.3% in mice with the TT genotype ( Fig.…”

MC4R mutant mice develop ovarian teratomas

“…Thus, a small fragment of the 129 strain was inserted in LT-Ter LT*/LT* . There is a possibility that other genes that prevent www.nature.com/scientificreports/ OTs have been known to develop from the parthenogenesis of oocytes 20,21 . Thus, we checked for this by observing sections prepared from mice that were expected to start to produce teratomas.…”

“…As a result of the generation of many genetically modified mice so far, it has been reported that ovarian teratomas also develop by different mechanisms. The onset of OTs due to parthenogenesis has been reported in mice in which the Mos gene has been knocked out, which has the function of meiotic arrest 21 . Yang et al showed that conditional knockout mice of retinoblastoma protein 1 (Rb1) developed ovarian teratomas and that abnormalities of somatic follicular cells also cause teratoma formation 15 .…”

Disrupted MOS signaling alters meiotic cell cycle regulation and the egg transcriptome

“…Initial analysis of the Mos knockout mice showed that a subset of eggs failed to maintain the metaphase II arrest and instead undergoes parthenogenetic activation and abnormal cell divisions (Colledge et al ., 1994; Hashimoto et al ., 1994). Furthermore, approximately one-third of mos -/- mice develop germ cell tumors over time, suggesting that the activated eggs remain in the ovary, instead of being ovulated, and then develop into tumors (Colledge et al ., 1994; Hashimoto et al ., 1994; Hirao and Eppig, 1997). These initial studies led us to further analyze the consequences of the loss of MOS during meiosis and in parthenogenesis.…”