The developmental potential of androgenones, gynogenones, and parthenogenones

Gynogenetic and Parthenogenetic embryos, with only maternally inherited genomes, and androgenetic embryos, with only a paternally inherited genome, fail to develop to term, and each fails in development in characteristic ways. This thesis defines the developmental potential of isoparental (androgenetic, parthenogenetic, and gynogenetic) cells. The construction of chimeras between single isoparental blastomeres and normal 8-cell embryos is described. The chimeras were allowed to develop to either the late blastocyst stage or the late gastrulating stage embryo, and then the tissue distribution of the isoparental component was analyzed. The isoparental embryos were derived from a transgenic mouse line carrying plasmid and mouse B-globin sequences. The isoparental cells were detected in histological sections of chimeras by DNA-DNA in situ hybridization to the transgene, using a biotinylated DNA probe, with an enzymatic detection system. There were significant differences in the tissue distributions for the androgenetic, parthenogenetic, and gynogenetic cells in chimeras at the gastrulating stage. Androgenetic cells contributed strongly to all trophectoderm derived tissues, with only a rare contribution to any tissues of the embryo proper, extraembryonic mesoderm, or extraembryonic endoderm. Parthenogenetic cells shared a similar developmental fate to gynegenetic cells, contributing to all tissues of the embryo proper and to the extraembryonic mesoderm, but only rarely to the extraembryonic endoderm or to any trophectoderm derived tissues. When the number of chimeric blastocysts were counted with a transgenic contribution to the inner cell mass (ICM), the trophectoderm, or both the ICM and trophectoderm, we found no statistically significant difference between the normal, parthenogenetic, and androgenetic chimeras. However, in those chimeras where there was a contribution by androgenetic cells to the ICM, the contribution was less than that seen by normal transgenic cells in control chimeras. Since androgenetic and parthenogenetic cells were present in chimeras at a high frequency in both the ICM and trophectoderm at the blastocyst stage, but not at late gastrulation, these cells must not respond normally to developmental signals subsequent to blastocyst formation and prior to late gastrulation