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          Institute: MPI für molekulare Genetik     Collection: Department of Human Molecular Genetics     Display Documents



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ID: 226099.0, MPI für molekulare Genetik / Department of Human Molecular Genetics
Divergent genetic and epigenetic post-zygotic isolation mechanisms in Mus and Peromyscus
Authors:Zechner, U.; Shi, W.; Hemberger, M.; Himmelbauer, Heinz; Otto, Sabine; Orth, A.; Kalscheuer, Vera M.; Fischer, Ute; Elango, R.; Reis, A.; Vogel, W.; Ropers, Hans-Hilger; Rüschendorf, F.; Fundele, Reinald
Language:English
Date of Publication (YYYY-MM-DD):2004-01-08
Title of Journal:Journal of Evolutionary Biology
Journal Abbrev.:J Evol Biol
Volume:17
Issue / Number:2
Start Page:453
End Page:460
Copyright:Blackwell Publishing, Inc.
Review Status:not specified
Audience:Experts Only
Abstract / Description:Interspecific hybridization in the rodent genera Peromyscus and Mus results in abnormal placentation. In the Peromyscus interspecies hybrids, abnormal allelic interaction between an X-linked locus and the imprinted paternally expressed Peg3 locus was shown to cause the placental defects. In addition, loss-of-imprinting (LOI) of Peg3 was positively correlated with increased placental size. As in extreme cases this placental dysplasia constitutes a post-zygotic barrier against interspecies hybridization, this finding was the first direct proof that imprinted genes may be important in speciation and thus in evolution. In the Mus interspecies hybrids, a strong role of an X-linked locus in placental dysplasia has also been detected. However, here we show by backcross and allele specific expression analyses that neither LOI of Peg3 nor abnormal interactions between Peg3 and an X-linked locus are involved in generating placental dysplasia in Mus hybrids, although the placental phenotypes observed in the two genera seem to be identical. In contrast to this, another dysgenesis effect common to Peromyscus and Mus hybrids, altered foetal growth, is caused at least in part by the same X-chromosomal regions in both genera. These findings first underline the strong involvement of the X-chromosome in the genetics of speciation. Secondly, they indicate that disruption of epigenetic states, such as LOI, at specific loci may be involved in hybrid dysgenesis effects in one group, but not in another. Thus, we conclude that even in closely related groups divergent molecular mechanisms may be involved in the production of phenotypically similar post-zygotic barriers against hybridization.
External Publication Status:published
Document Type:Article
Communicated by:Hans-Hilger Ropers
Affiliations:MPI für molekulare Genetik
External Affiliations:Institute for Human Genetics, Johannes Gutenberg-University Mainz, Langenbeckstr, Mainz, Germany;
Department of Development and Genetics, Uppsala University, Norbyvägen, Uppsala, Sweden;
Laboratory of Genomes and Populations, University of Montpellier, Place Eugène Bataillon C.C., Montpellier, France;
Discovery Bioinformatics, GlaxoSmithKline, Gunnels Wood Road, Stevenage SG1 2NY, UK;
Molecular Genetics and Gene Mapping Center, Max-Delbrück-Center, Robert-Rössle-Strasse, Berlin, Germany;
Department of Human Genetics, University of Ulm, Ulm, Germany;
Institute for Medical Biometry, Informatics and Epidemiology, Rheinische Friedrich-Wilhelms-University, Bonn, Germany.
Identifiers:ISSN:1420-9101
DOI:10.1046/j.1420-9101.2003.00656.x
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