| First Author | Hirao Y | Year | 1997 |
| Journal | Mol Reprod Dev | Volume | 48 |
| Issue | 3 | Pages | 391-6 |
| PubMed ID | 9322252 | Mgi Jnum | J:43317 |
| Mgi Id | MGI:1097497 | Doi | 10.1002/(SICI)1098-2795(199711)48:3<391::AID-MRD13>3.0.CO;2-Z |
| Citation | Hirao Y, et al. (1997) Parthenogenetic development of Mos-deficient mouse oocytes. Mol Reprod Dev 48(3):391-6 |
| abstractText | 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. |
