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

MPS-Authors

Véron,  Nathalie
Max Planck Society;

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Bauer,  Hermann
Dept. of Developmental Genetics (Head: Bernhard G. Herrmann), Max Planck Institute for Molecular Genetics, Max Planck Society;

Lüder,  Gerhild
Max Planck Society;

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Werber,  Martin
Dept. of Developmental Genetics (Head: Bernhard G. Herrmann), Max Planck Institute for Molecular Genetics, Max Planck Society;

Herrmann,  Berhard G.
Max Planck Society;

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Citation

Véron, N., Bauer, H., Weiße, A. Y., Lüder, G., Werber, M., & Herrmann, B. G. (2009). Retention of gene products in syncytial spermatids promotes non-Mendelian inheritance as revealed by the t complex responder. Genes and Development, 23(23), 2705-2710. doi:10.1101/gad.553009.


Cite as: https://hdl.handle.net/11858/00-001M-0000-0010-7CBB-C
Abstract
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.