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Aneuploid correction and confined placental mosaicism.

Uniparental disomy (UPD) can be caused by various genetic mechanisms such as gamete complementation, chromosome duplication in a monosomic zygote or postzygotic aneuploid correction. This latter mechanism has been recently well documented in human reproduction and seems to be strictly related to placental mosaicism. We have therefore studied some aspects of confined placental mosaicism (CPM) which are useful to clarify one of the most common sources of UPD in humans. Abnormal distribution of chromosomes in postzygotic mitotic cell divisions may result in a mosaic condition with two or more cell lines showing different chromosome constitutions. The effects on fetal phenotype and pregnancy development depend on the chromosomes involved, the distribution of the abnormal cells among tissues and on the precise stage at which chromosome mutation occurs. As shown in Fig. 1, when the mutational event occurs in the blastocyst, prior to the differentiation of embryonic and chorionic compartments, the mosaicism is found in both the placental and fetal tissues. In contrast, when the chromosome mutation occurs at a later stage, after embryonic and chorionic compartment separation, the abnormal cells may be confined to the placenta or to the embryo, and are not necessarily found in both. The possibility that mosaicism might be confined to extraembryonic tissue was first suggested by Ford [2] in 1969 who described an aneuploid cell line in the fetal membrane of the mouse. In 1978, Warburton et al. [3] found an unexpectedly high frequency of mosaic autosomal trisomies in cultures from spontaneous abortions. They suggested that these findings, as well as the relatively high rate of mosaicism in amniotic fluid cell cultures, which are usually not confirmed in the newborn, could be related to cells of extra-fetal origin. In fact, as reported by Priest et al. [4] in 1977,