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Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-1805

Behrens, A; Genoud, N; Naumann, H; Rülicke, T J; Janett, F; Heppner, F L; Ledermann, B; Aguzzi, A (2002). Absence of the prion protein homologue Doppel causes male sterility. EMBO Journal, 21(14):3652-3658.

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Abstract

The agent that causes prion diseases is thought to be identical with PrP(Sc), a conformer of the normal prion protein PrP(C). PrP(C)-deficient mice do not exhibit major pathologies, perhaps because they express a protein termed Dpl, which shares significant biochemical and structural homology with PrP(C). To investigate the physiological function of Dpl, we generated mice harbouring a homozygous disruption of the Prnd gene that encodes Dpl. Dpl deficiency did not interfere with embryonic and postnatal development, but resulted in male sterility. Dpl protein was expressed at late stages of spermiogenesis, and spermatids of Dpl mutants were reduced in numbers, immobile, malformed and unable to fertilize oocytes in vitro. Mechanical dissection of the zona pellucida partially restored in vitro fertilization. We conclude that Dpl regulates male fertility by controlling several aspects of male gametogenesis and sperm-egg interaction.

Item Type:Journal Article, refereed
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Institute of Neuropathology
DDC:570 Life sciences; biology
610 Medicine & health
Language:English
Date:2002
Deposited On:11 Feb 2008 13:25
Last Modified:07 Jan 2014 18:15
Publisher:Nature Publishing Group
ISSN:0261-4189
Publisher DOI:10.1093/emboj/cdf386
PubMed ID:12110578
Citations:Web of Science®. Times Cited: 98
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