DDK

Inbr: F105. Albino. Genet: A,B,c,D,s. Developed by K. Kondo from outbred dd stock from Institute of Infectious Diseases, University of Tokyo, in 1944.

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Characteristics

DDK females mated to C57BL males are semi-sterile, but the reciprocal cross is fully fertile. The low `fertility' is caused by embryonic death at the morula-blastocyst or pre-egg cylinder stage 3-5 days after fertilisation. A deficit of trophoblast formation was observed. Transplantation experiments show that the defect is the property of the embryos, not the uterine environment. The DDK karyotype appears normal (Wakasugi, 1973). Tendency to diabetes (Nishimura, 1969). Nuclear transplantation experiments between hybrid eggs of BALB/c and DDK strains has shown that failure of F1 (DDK female x BALB/c male) embryos to develop is not due to the combination per se of maternal (DDK) and paternal (BALB/c) genomes but rather to an incompatibility between paternal (BALB/c) genomic contribution and DDK cytoplasm. This incompatibility does not occur between a female BALB/c pronucleus and the DDK cytoplasm, suggesting the involvement of a differential imprinting of parental genomes. (Babinet et al 1990)

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Babinet C., Richoux V., Guenet J. L., and Renard J. P. (1990) The DDK inbred strain as a model for the study of interactions between parental genomes and egg cytoplasm in mouse preimplantation development. Development - Supplement 1990, 81-87.

Nishimura M. (1969) Breeding of mice strains for diabetes mellitus. Exp. Animals (Japan) 18, 147-157.

Wakasugi N. (1973) Studies on fertility of DDK mice: reciprocal crosses between DDK and C57BL/6J strains and experimental transplantation of the ovary. J. Reprod. Fertil. 33, 283-291.

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INBRED STRAINS OF MICE
Updated 9 Apr. 1998
Michael FW Festing
MRC Toxicology Unit, Hodgkin Building,
University of Leicester, UK