Retention of gene products in syncytial spermatids promotes non-Mendelian inheritance as revealed by the t complex responder.
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.
Véron
Nathalie
N
Department of Developmental Genetics, Max-Planck-Institute for Molecular Genetics, 14195 Berlin, Germany.
Bauer
Hermann
H
Weisse
Andrea Y
AY
Lüder
Gerhild
G
Werber
Martin
M
Herrmann
Bernhard G
BG
D000818:Animals; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D040582:Inheritance Patterns / Q000235:genetics*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D008969:Molecular Sequence Data; D010641:Phenotype; D011494:Protein Kinases / Q000235:genetics* / Q000378:metabolism*; D013087:Spermatids / Q000378:metabolism* / Q000648:ultrastructure
D011494:Protein Kinases; C403405:Smok1 protein, mouse