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Review
. 2007 Sep;49(7):555-9.
doi: 10.1111/j.1440-169X.2007.00952.x. Epub 2007 Jul 17.

Embryologic, cytobiologic and genetic interpretations of DDK syndrome in mice

Affiliations
Review

Embryologic, cytobiologic and genetic interpretations of DDK syndrome in mice

Noboru Wakasugi. Dev Growth Differ. 2007 Sep.

Abstract

DDK syndrome is known as embryonic death at the morula-blastocyst stage in female mice of the DDK strain mated with males from other strains (alien males). The embryonic death is interpreted to be caused by incompatibility between oocyte factors and the product from male pronucleus, both of which are under the control of alleles at the same locus on Chromosome 11. This review explains the hypothesis proposing that the embryonic death may be caused primarily by failure in de novo regeneration of centrosomes containing centrioles in the trophectodermal cells. Centrioles disintegrate during gametogenesis in mice, and new centrioles are formed after the cleavage stage during which cell division proceeds with the microtubule organizing center having no centrioles. The failure in de novo regeneration of the centrosomes may arrest cell division and consequently result in embryonic death. Another aspect of DDK syndrome is distortion of the second polar body extrusion in the semi-incompatible cross. In the heterozygous (DDK/alien) oocytes fertilized with alien spermatozoa, DDK allele is more frequently retained in the oocyte nucleus, and alien allele tends to be carried into the polar body. This distortion may possibly be caused by derangement in the spindle system. Therefore, both aspects of DDK syndrome can be regarded as being derived from the abnormality in the centrosome-spindle system according to this hypothesis.

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