Reinald Fundele
Max-Planck Institute for Molecular Genetics
Interspecific hybridization in mammals results in several consistent hybrid dysgenesis (HD) effects, most notably male sterility and abnormal growth (1). It can be assumed that other, less obvious HD effects also occur. Indeed, in those interspecific hybrids where this has been assessed to date, abnormal placental development was observed. Interspecific hybrid placental dysplasia (IHPD) was analyzed in some detail in the two rodent genera Peromyscus and Mus (2) and strong similarities were detected between these groups. Reciprocal placental phenotypes, hypoplasia or hyperplasia, appeared in reciprocal matings; the placental tissue that was mainly affected was the spongiotrophoblast; and placental dysplasia exhibited genetic linkage to the X-chromosome. In Peromyscus only, involvement of the autosomal imprinted, paternally expressed gene gin the generation of placental hyperplasia was demonstrated (3). The pronounced similarities between Peromyscus and Mus hybrid placental dysplasias suggested that Peg3, or at least loci linked to Peg3, should also be involved in placental hyperplasia in Mus. However, our study, which combined BC analysis, allelic expression (loss-of-imprinting) analysis, and the use of BC males heterozygous at the Peg3 locus, does not support a major role of this imprinted gene in murine IHPD. This finding suggests that different molecular mechanisms have been recruited in comparatively closely related rodent groups to produce indiscernible HD phenotypes. However, our BC analysis has shown that another imprinted chromosome region exhibits linkage to placental hyperplasia. In addition, we have evidence that loss-of-imprinting is involved in another HD effect, that is, postnatal growth.
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