Submission Number: HID-4-25-22

Abstract Number: 373

COMPARISON OF THE DEVELOPMENT OF ANDROGNETIC AND PARTHENOGENETIC MOUSE EMBRYOS.

Hidenori Akutsu ¹, Hiroyuki Tateno ^1,2, Hirokazu Kusakabe ¹ and Ryuzo Yanagimachi* ¹

Department of Anatomy and Reproductive Biology, University of Hawaii Medical School, Honolulu, HI, USA ¹
Department of Biological Sciences, Asahikawa Medical College, Asahikawa, Japan ²

Abstract:
Normal development in mammals requires the differential expression of maternal and paternal genomes and is considered to be the primary reason why embryos of androgenetic, parthenogenetic and gynogenetic origin are unable to develop to term. We have compared preimplantation development of haploid and diploid androgenetic and parthenogenetic mouse embryos in vitro. Gametes were obtained from superovulated, 8 to 12 week old, B6D2F1 hybrid females. Haploid parthenogenetic embryos were produced by activating mature oocytes (collected 14h post hCG) with 10 mM Sr²⁺ for 6 hr and diploid parthenogenetic embryos by suppressing the extrusion of PB2 with cytochalasin B(5 g/ml) during activation. Haploid and diploid androgenetic embryos were generated by removing the MII spindle from mature oocytes before 1 or 2 sperm heads. 94% (122/130) diploid and 52% (86/165) haploid parthenogenetic embryos developed to blastocysts compared with only 49% (304/620) of diploid and 9% (39/455) of haploid androgenetic embryos. The majority of haploid androgenetic embryos arrested at the 4-cell stage. Chromosomal analysis of haploid parthenogenetic (n=103) and androgenetic (n=123) embryos at 1st or 2nd cleavage division showed that 93-94% had normal chromosome complements. Embryos lacking X-chromosome(s) fail to develop beyond 8 cells. Thus, only 75% diploid and 50% haploid androgenetic embryos would be expected to develop into blastocysts. The present data indicate that the activity the X-chromosome is dependent upon parental origin: the later activation of the paternal X-chromosome compromises early embryonic development. The lower developmental potential of haploid embryos probably reflects deficiencies in expression of other autosomal genes, which is more severe when the autosomes are of paternal origin. Our data suggest that the effects of genetic imprinting during gamete formation are already apparent during the early stages of embryonic genome activation. .

Keywords: androgenesis parthenogenesis mouse preimplantation development

This abstract is being presented at: 8:00 AM in session:
Preimplantation Embryo/Fetus