Abstract
PARTHENOGENESIS occurs spontaneously in about 10% of ovulated eggs of inbred strain LT/Sv mice1,2 and is experimentally inducible in other strains by various physical and chemical agents (see ref. 3 for review). The development of most parthenotes seems normal up to the expanded blastocyst stage4. They implant in the uterus, but, for reasons unknown, are resorbed within a few days. Although they rarely survive to 8 d of gestation when they develop somites, heart muscle, amnion, and neuroepithelium, Kaufman et al.5 obtained two embryos with 25 somites by transferring parthenogenetic blastocysts to the uteri of ovariectomised females treated with exogenous hormones. Even though parthenogenetic embryos do not survive to birth, their cells contain genetic information that permits prolonged survival. If two-cell parthenotes are cultured to the blastocyst stage and then grafted to extrauterine sites such as the testis or kidney, they may survive as teratomas composed of several types of tissues and undifferentiated embryonal cells (refs 1, 6 and L.C.S. and D.S.V., unpublished). Furthermore, strain LT/Sv spontaneous ovarian teratomas contain numerous differentiated tissues composed of parthenogenetically derived cells. The questions remains—why do parthenotes not survive at the organismic level in utero? Eicher and Hoppe7 used experimental chimaeras composed of normal and abnormal embryos to transmit a recessive X-linked lethal mutation, and we considered the possibility that parthenogenetic embryonic cells might also be rescued if combined with normal embryonic cells. Here we present evidence of production of at least two viable chimaeras between normal and parthenogenetic embryos.
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References
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STEVENS, L., VARNUM, D. & EICHER, E. Viable chimaeras produced from normal and parthenogenetic mouse embryos. Nature 269, 515–517 (1977). https://doi.org/10.1038/269515a0
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DOI: https://doi.org/10.1038/269515a0
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