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

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.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0010-7CBB-C Version Permalink: http://hdl.handle.net/11858/00-001M-0000-0010-7CBC-A
Genre: Journal Article
Alternative Title : Genes Dev

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 Creators:
Véron, Nathalie1, Author
Bauer, Hermann2, Author              
Weiße, Andrea Y., Author
Lüder, Gerhild1, Author
Werber, Martin2, Author              
Herrmann, Berhard G.1, Author
Affiliations:
1Max Planck Society, ou_persistent13              
2Dept. of Developmental Genetics (Head: Bernhard G. Herrmann), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433548              

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Free keywords: Mouse; t haplotype; Non-Mendelian inheritance; Transmission ratio distortion; Spermatogenesis; Motility
 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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Language(s): eng - English
 Dates: 2009-12-01
 Publication Status: Published in print
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Method: -
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Title: Genes and Development
  Alternative Title : Genes Dev
Source Genre: Journal
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Affiliations:
Publ. Info: -
Pages: - Volume / Issue: 23 (23) Sequence Number: - Start / End Page: 2705 - 2710 Identifier: ISSN: 0890-9369