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Journal Article

Disruption of spermatogenesis in mice lacking A-type lamins

MPS-Authors

Liebe,  Bodo
Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons50515

Scherthan,  Harry
Dept. of Human Molecular Genetics (Head: Hans-Hilger Ropers), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Citation

Alsheimer, M., Liebe, B., Sewell, L., Stewart, C. L., Scherthan, H., & Benavente, R. (2004). Disruption of spermatogenesis in mice lacking A-type lamins. Journal of Cell Science, 117(7), 1173-1178.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0010-88A7-8
Abstract
Nuclear lamins are structural protein components of the nuclear envelope. Mutations in LMNA, the gene coding for A-type lamins, result in several human hereditary diseases, the laminopathies, which include Emery-Dreifuss muscular dystrophy, dilated cardiomyopathy, familial partial lipodystrophy and Hutchinson-Gilford progeria. Similar to the human conditions, it has been shown that Lmna–/– mice develop severe dystrophies of muscle and fat tissues. Here we report that Lmna–/– mice display impaired spermatogenesis, with a significant accumulation of spermatocytes I during early prophase I stages, while pachytene spermatocytes are severely defective in synaptic pairing of the sex chromosomes in particular, leading to massive apoptosis during the pachytene stage of meiosis I. In contrast, oogenesis remains largely unaffected in Lmna–/– mice. These results reveal A-type lamins as important determinants of male fertility.