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First published online March 2, 2004
doi: 10.1242/10.1242/jcs.00975

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Disruption of spermatogenesis in mice lacking A-type lamins

Manfred Alsheimer^1,*, Bodo Liebe^2,*, Lori Sewell³, Colin L. Stewart³, Harry Scherthan^2, and Ricardo Benavente^1,

¹ Department of Cell and Developmental Biology, Biocenter, University of Würzburg, Am Hubland, 97074 Würzburg, Germany
² Max-Planck-Institute for Molecular Genetics, 14195 Berlin, Germany
³ Cancer and Developmental Biology Laboratory, National Cancer Institute, Frederick, MD 21702-1201, USA

Authors for correspondence (e-mail: benavente{at}biozentrum.uni-wuerzburg.de, schertha{at}molgen.mpg.de)

Accepted 11 November 2003

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.

Key words: Spermatogenesis, Meiosis, Nuclear lamins, LMNA

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