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Molecular Human Reproduction, Vol. 7, No. 6, 513-520, June 2001
© 2001 European Society of Human Reproduction and Embryology


Testis and spermatogenesis

Teratozoospermia in mice lacking the transition protein 2 (Tnp2)

Ibrahim M. Adham1, Karim Nayernia1, Elke Burkhardt-Göttges1, Özlem Topaloglu1, Christa Dixkens1, Adolf F. Holstein2 and Wolfgang Engel1,3

1 Institute of Human Genetics, University of Göttingen, D-37073 Göttingen and 2 Department of Anatomy, Eppendorf University Hospital, D-20251 Hamburg, Germany

Abstract

It is believed that the transition proteins (Tnp1 and Tnp2) participate in the removal of the nucleohistones and in the initial condensation of the spermatid nucleus. Later in spermatogenesis, Tnp1 and Tnp2 are replaced by the protamines 1 and 2. In an effort to elucidate the physiological role of Tnp2, we have disrupted its locus by homologous recombination. Breeding of the Tnp2–/– males on different genetic backgrounds revealed normal fertility on the mixed background C57BL/6Jx129/Sv, but total infertility on the inbred 129/Sv background. Light and electron microscopy showed that the germ cells were capable of undergoing chromatin condensation, although many spermatozoa exhibited head abnormalities with acrosomes not attached to the nuclear envelope. Furthermore, migration of Tnp2–/– spermatozoa from the uterus into the oviduct was reduced. These results suggest that male infertility of the Tnp2–/– mice is a result of sperm head abnormalities and reduced sperm motility. The increased level of the Tnp1 transcript in testes of the Tnp2-deficient mice raises the possibility that a deficiency created through the disruption of the Tnp2 gene can be compensated for by recruitment of the Tnp1.

acrosome/chromatin condensation/genetic background/teratozoospermia/Tnp2

Notes

3 To whom correspondence should be addressed at: Institute of Human Genetics, University of Göttingen D-37073 Göttingen, Germany. E-mail: wengel{at}gwdg.de


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