[Role of various portions of chromosome 17 in the early embryogenesis of the laboratory mouse].

Peculiarities of the early development of mice embryos with structural aberrations of chromosome 17 were studied in mice heterozygous for reciprocal translocations T (16; 17) 43H and T (9; 17) 138Ca. Deficiency for the distal part of chromosome 17 corresponding to the E-region (Df 17 E1-E5), as well as deficiency for its most proximal part, the AB region (Df 17 A1-A-3, B) carrying all genes of complex T-locus, does not block cleavage, blastulation and implantation but severely affects immediate postimplantation development and causes embryonic death during early neurulation. Deficiency for the middle part of chromosome 17, including Giemsa-positive band 17C and the most of Giemsa-negative band D, becomes evident just after a few cleavage divisions and all these embryos die at the morula stage (8-16 blastomeres). It has been concluded that genes of the CD region in chromosome 17 are of major importance for genetic control of the early development in laboratory mice. The possible causes for early embryonic death are discussed in connection with the genetic map of chromosome 17 and a hypothesis of mutual activation of homologous autosomes and their segments at initial stages of embryogenesis is suggested.