[Trisomy of an autosome in mice heterozygous by a Robertson translocation]

From 866 embryos of mice heterozygous by Roberstsonian translocations 54 ones (6,2%) had trisomy of one of translocated chromosomes. The frequency of trisomy is unique for each translocation, dependent on other chromosomal redistributions in the karyotype and on sex of heterozygous individuals. Trisomy of all the autosomes studied (N 1, 5, 8, 9, 14, 15, 17, 19) results in a characteristic complex of non-specific malformations which includes general delay in development, reduction of the cephalic portion of the nervous tube, cranio-fascial malformations, hypertrophy of the heart cavities. In a number of cases autosomal trisomy (N 15,8) is responsible for certain specific disturbances of morphogenesis. The excess of majority of autosomes (N 5, 8, 9, 15, 16 and 17) causes death of embryos in the period of active organogenesis. Embryos with trisomy of the 1st, 14th and 19th pairs of autosomes in certain cases reach the fetal period but have severe malformations and are non-survival. In mice karyotype there seems to be no autosomes whose trisomy is compatible with postnatal development. Signs of similarity and difference in manifestation of numericle chromosomal aberrations were noted in embryogenesis of mice and man. Principle possibility of modelling chromosomal embryopathy of man in mice with Robertsonian translocations is supposed.