Retention of gene products in syncytial spermatids promotes non-Mendelian inheritance as revealed by the t complex responder
- Nathalie Véron1,2,
- Hermann Bauer1,
- Andrea Y. Weiße3,6,
- Gerhild Lüder4,
- Martin Werber1,5 and
- Bernhard G. Herrmann1,5,7
- 1Department of Developmental Genetics, Max-Planck-Institute for Molecular Genetics, 14195 Berlin, Germany;
- 2Faculty of Biology, Free University Berlin, 14195 Berlin, Germany;
- 3Department of Mathematics and Computer Science, Biocomputing Group, Free University Berlin, 14195 Berlin, Germany;
- 4Electron Microscopy Group, Max-Planck-Institute for molecular Genetics, 14195 Berlin, Germany;
- 5Institute for medical Genetics-CBF, Charité-University Medicine Berlin, 12203 Berlin, Germany
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.
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Footnotes
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↵7 Corresponding author.
E-MAIL herrmann{at}molgen.mpg.de; FAX 49-30-8413-1229.
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Article is online at http://www.genesdev.org/cgi/doi/10.1101/gad.553009.
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Supplemental material is available at http://www.genesdev.org.
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- Received August 14, 2009.
- Accepted October 12, 2009.
- Copyright © 2009 by Cold Spring Harbor Laboratory Press
