In the chromosome complement of Bos taurus, the large X and small Y are both metacentric while the remaining 29 autosomal pairs are all acrocentric, a karyological characteristic which permits unequivocal differentiation of 2 A-XX cells from 2A-XY cells at mitotic metaphase. In this study, seven Holstein-Freisian calves less than one day old were utilized. One bull and one heifer, normal and single-born, served as controls. In the remaining three freemartins and two bull twins, blood chimerism was determined cytologically. In the testes of the two bull twins, 2 A-XX cells were also detected. In fact, twice as many 2 A-XX as 2A-XY cells were found in the histologically normal testis of one animal. Whether or not these 2 A-XX cells were germ cells capable of functioning as spermatogonia could not be ascertained. In the free-martin gonads, there was no evidence of propagation of 2 A-XY cells.
To gain further insight into the mechanism of induction of dominant lethal mutations, the relationship between chromosome aberrations in bone marrow and in male germ cells after treatment with mitomycin C (MMC) and ethyl methanesulfonate (EMS) was examined. In addition, we obtained fertilized eggs from the oviducts of crossbred female mice in the same way as in the dominant lethal mutation test, and examined chromosome aberrations in male pronuclei. MMC 2.5 and 5.0 mg/kg, EMS 175 and 350 mg/kg were given subcutaneously to slc-ICR mice. It was concluded that MMC causes a decrease in the sperm count by killing germ cells, which in turn causes an increase in the number of unfertilized eggs and preimplantation egg loss. MMC seems also to cause invisible damages in the chromosomes of spermatocytes which lead to dominant lethality. EMS induced chromosome damage in the post-meiotic germ cells, and this damage, in turn, produced chromosome aberrations in the eggs, resulting in a high incidence of dominant lethality.
We examined the effects of mitomycin C and aminopterin on ovulation in vivo and, fertilization, subsequent cleavage and implantation in slc-ICR female mice using methods of fertilization and culture in vitro. Chemicals were injected into mice at the MI (meiosis I) stage or 3 hours before the MI stage in order to examine their toxicity. Mitomycin C did not affect ovulation, but decreased the rate of fertilization. A high dose of mitomycin C (4 mg/kg) inhibited fertilization and the development of ova to the 2-cell stage. Aminopterin affected neither ovulation nor fertilization. At either the MII (meiosis II) stage or 3 hours before the MII stage, high doses (4 and 2 mg/kg) of mitomycin C arrested cleavage and implantation. The cleavage was blocked frequently between the 3-4 cell stage and the 5-8 cell stage. Aminopterin affected neither cleavage nor implantation.
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