The gametic and zygotic selection of genome imbalance was investigated in the Chinese hamster by direct chromosome analyses of spermatocytes and preimplantation embryos from crosses between chromosomally normal females and males heterozygous for a reciprocal translocation, T(2;10)3Idr, abbreviated here as T3. The karyotypes and the frequencies of embryos observed at the first cleavage in the cross + / + ♀ × T3/ + ♂ were consistent with those expected from Mil scoring in male T3 heterozygotes. Therefore, it was concluded that there was neither gametic selection against genome imbalance nor zygotic selection from fertilization until the first cleavage metaphase. However, 9.1–10.8% of embryos were arrested at the two-cell stage, and karyotypes of these embryos were confirmed as 22(2,10,10,102), 21(2,10,10), and 21(2,10,102). The common abnormality of these embryos was partial monosomy of chromosome 2. Among day 4 embryos, some chromosomally unbalanced embryos, mainly with a deficiency of other segments of chromosomes 2 and 10, had fewer blastomeres than chromosomally balanced embryos. This finding suggests that cleavage of these embryos had been retarded by day 4 of gestation.
The hormonal requirements for ovum implantation vary among species; at least in the mouse and rat, progesterone and estrogen, of which production and secretion are controlled along the hypothalamo‐pituitary‐ovarian axis, are indispensable for the initiation of an implantation. In fact, implantation of the blastocyst in these species is delayed or prevented by not only ovariectomy, but also by: hypophysectomy, lesion of the median eminence or a treatment of the maternal organism with an agent that interferes with this endocrine control system. The preimplantation developmental events such as cleavage, blastocyst formation and shedding of the zona pellucida and gestational changes of the uterine luminal epithelium are delayed under a few conditions causing a delayed implantation. Experimental data suggesting that uterine changes leading to the formation of a ‘receptive’ endometrium are hormone‐dependent are accumulating. Thus, the observed delay in changes in the uterine epithelium may be attributed to the alteration of the endocrine control. In contrast, it is difficult to determine how the delay in embryonic development occurs. Among the conceivable explanations are: the direct effect on embryos (ova) of implantation‐delaying factors, a mechanism synchronizing embryonic development with the uterine change or disturbance of possible hormonal control over the embryonic development.
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