Retention of gene products in syncytial spermatids promotes non-Mendelian inheritance as revealed by the t complex responder.

Nathalie Véron, Hermann Bauer, Andrea Y Weisse, Gerhild Lüder, Martin Werber, Bernhard G Herrmann

Department of Developmental Genetics, Max-Planck-Institute for Molecular Genetics, 14195 Berlin, Germany.

Genes & development 2009 Dec 1

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The t complex responder (Tcr) encoded by the mouse t haplotype is able to cause phenotypic differences between t and + sperm derived from t/+ males, leading to non-Mendelian inheritance. This capability of Tcr contradicts the concept of phenotypic equivalence proposed for sperm cells, which develop in a syncytium and actively share gene products. By analyzing a Tcr minigene in hemizygous transgenic mice, we show that Tcr gene products are post-meiotically expressed and are retained in the haploid sperm cells. The wild-type allele of Tcr, sperm motility kinase-1 (Smok1), behaves in the same manner, suggesting that Tcr/Smok reveal a common mechanism prone to evolve non-Mendelian inheritance in mammals.

Citation

Nathalie Véron, Hermann Bauer, Andrea Y Weisse, Gerhild Lüder, Martin Werber, Bernhard G Herrmann. Retention of gene products in syncytial spermatids promotes non-Mendelian inheritance as revealed by the t complex responder. Genes & development. 2009 Dec 1;23(23):2705-10