Chromosomal control of early embryonic development in mice: II. Experiments on embryos with structural aberrations of autosomes 7, 9, 14 and 17

Abstract

SUMMARYPerculiarities of preimplantation and early postimplantation development were studied in embryos with partial deletions and duplications of chromosomes 7, 9, 14 and 17, in the progeny of mice heterozygous for the unequal reciprocal translocations T(7; 14)2Iem, T(16; 17)43H and T(9; 17)138Ca. Deficiencies for any part of autosomes 9 or 14 combined with duplications of the corresponding segments of autosomes 7 or 17 do not affect preimplantation development, though they are lethal soon after implantation. Deficiency for the distal part of chromosome 7 (Df7F4) induces embryonic death by the early blastocyst stage. Deficiencies for the distal part of chromosome 17 (Df17El–E5), as well as for its proximal region (Df17AB) carrying all genes of theT-tcomplex, have no detrimental effects on cleavage, blastulation and implantation, but are lethal after implantation, mostly during early neurulation. Deficiency for the middle part of chromosome 17 (Df17CD) is expressed just after a few cleavage divisions, and these embryos all die by the morula stage. It is suggested that the genes of the CD region of chromosome 17 and of the F4 region of chromosome 7 are of major significance for genetic control of early development in the laboratory mouse.