First Author | Baldacci PA | Year | 1992 |
Journal | Mamm Genome | Volume | 2 |
Issue | 2 | Pages | 100-5 |
PubMed ID | 1347470 | Mgi Jnum | J:4627 |
Mgi Id | MGI:53112 | Doi | 10.1007/BF00353857 |
Citation | Baldacci PA, et al. (1992) The locus Om, responsible for the DDK syndrome, maps close to Sigje on mouse chromosome 11. Mamm Genome 2(2):100-5 |
abstractText | The DDK inbred strain of mouse has a striking particularity: when DDK females are crossed to males of other strains they exhibit a reduced fertility, whereas the reciprocal crosses (non-DDK females x DDK males) are fertile (Wakasugi et al. 1967; Wakasugi 1973). The low fertility results from an early embryonic lethality, the F1 embryos dying near the late morula-early blastocyst stage. Genetic analyses (Wakasugi 1974) and nuclear and cytoplasmic transfers (Renard and Babinet 1986; Babinet et al. 1990; Mann 1986), have shown that the failure of the embroys to develop is due to an incompatibility between a DDK maternally encoded cytoplasmic product and the non-DDK paternal genome. In order to elucidate the genetic determinism of this embryonic lethality, we have analyzed the fertility of male progeny from a backcross BALB/c females x (BALB/c x DDK)F1 males and that of males from a set of recombinant inbred (RI) strains, established from DDK and BALB/c progenitors, when mated with DDK females. Our results indicate that a single locus, Om, is responsible for the DDK syndrome and is located on Chromosome (Chr) 11, very close to the Sigje locus. |