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Molecular and Cellular Biology, June 2005, p. 4892-4902, Vol. 25, No. 12
0270-7306/05/$08.00+0     doi:10.1128/MCB.25.12.4892-4902.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Normal Sexual Development and Fertility in testatin Knockout Mice

Virpi Töhönen,1,2,{dagger} Jessica Frygelius,1,{dagger} Majid Mohammadieh,3 Ulrik Kvist,3 Lauri J. Pelliniemi,4 Kevin O'Brien,5 Katarina Nordqvist,2,{dagger},{ddagger} and Anna Wedell1,{dagger}*

Department of Molecular Medicine, Karolinska Institutet/Karolinska University Hospital, SE-171 76 Stockholm, Sweden,1 Department of Cell and Molecular Biology, Medical Nobel Institute, Karolinska Institutet, SE-171 77 Stockholm, Sweden,2 Andrology Center, Department of Medicine, Karolinska Institutet/Karolinska University Hospital, Stockholm, Sweden,3 Laboratory of Electron Microscopy, University of Turku, FIN-20520 Turku, Finland,4 Center for Genomics and Bioinformatics, Karolinska Institutet, Stockholm, Sweden5

Received 11 October 2004/ Returned for modification 7 December 2004/ Accepted 10 March 2005

The testatin gene was previously isolated in a screen focused on finding novel signaling molecules involved in sex determination and differentiation. testatin is specifically upregulated in pre-Sertoli cells in early fetal development, immediately after the onset of Sry expression, and was therefore considered a strong candidate for involvement in early testis development. testatin expression is maintained in the adult Sertoli cell, and it can also be found in a small population of germ cells. Testatin shows homology to family 2 cystatins, a group of broadly expressed small secretory proteins that are inhibitors of cysteine proteases in vitro but whose in vivo functions are unclear. testatin belongs to a novel subfamily among the cystatins, comprising genes that all show expression patterns that are strikingly restricted to reproductive tissue. To investigate a possible role of testatin in testis development and male reproduction, we have generated a mouse with targeted disruption of the testatin gene. We found no abnormalities in the testatin knockout mice with regard to fetal and adult testis morphology, cellular ultrastructure, body and testis weight, number of offspring, spermatogenesis, or hormonal parameters (testosterone, luteinizing hormone, and follicle-stimulating hormone).


* Corresponding author. Mailing address: Department of Molecular Medicine, Karolinska Institutet, CMM:02, S-171 76 Stockholm, Sweden. Phone: 46 8 5177 65 35. Fax: 46 8 5177 36 20. E-mail: Anna.Wedell{at}cmm.ki.se.

{dagger} V.T., J.F., K.N., and A.W. contributed equally to this work.

{ddagger} Present address: VINNOVA, SE-101 58 Stockholm, Sweden.


Molecular and Cellular Biology, June 2005, p. 4892-4902, Vol. 25, No. 12
0022-538X/05/$08.00+0     doi:10.1128/MCB.25.12.4892-4902.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.




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