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Molecular and Cellular Biology, May 2006, p. 3595-3609, Vol. 26, No. 9
0270-7306/06/$08.00+0     doi:10.1128/MCB.26.9.3595-3609.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Loss of TSLC1 Causes Male Infertility Due to a Defect at the Spermatid Stage of Spermatogenesis{dagger}

Louise van der Weyden,1 Mark J. Arends,2 Oriane E. Chausiaux,3 Peter J. Ellis,3 Ulrike C. Lange,4 M. Azim Surani,4 Nabeel Affara,3 Yoshinori Murakami,5 David J. Adams,1 and Allan Bradley1*

Mouse Genomics Lab, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Cambridge, United Kingdom,1 Department of Pathology, University of Cambridge, Addenbrooke's Hospital, Cambridge, United Kingdom,2 Human Molecular Genetics Group, Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge, United Kingdom,3 Wellcome Trust/Cancer Research UK Gurdon Institute, The Henry Wellcome Building of Cancer and Developmental Biology, Tennis Court Road, Cambridge, United Kingdom,4 Tumor Suppression and Functional Genomics Project, National Cancer Center Research Institute, Tokyo, Japan5

Received 5 August 2005/ Returned for modification 1 October 2005/ Accepted 30 January 2006

Tumor suppressor of lung cancer 1 (TSLC1), also known as SgIGSF, IGSF4, and SynCAM, is strongly expressed in spermatogenic cells undergoing the early and late phases of spermatogenesis (spermatogonia to zygotene spermatocytes and elongating spermatids to spermiation). Using embryonic stem cell technology to generate a null mutation of Tslc1 in mice, we found that Tslc1 null male mice were infertile. Tslc1 null adult testes showed that spermatogenesis had arrested at the spermatid stage, with degenerating and apoptotic spermatids sloughing off into the lumen. In adult mice, Tslc1 null round spermatids showed evidence of normal differentiation (an acrosomal cap and F-actin polarization indistinguishable from that of wild-type spermatids); however, the surviving spermatozoa were immature, malformed, found at very low levels in the epididymis, and rarely motile. Analysis of the first wave of spermatogenesis in Tslc1 null mice showed a delay in maturation by day 22 and degeneration of round spermatids by day 28. Expression profiling of the testes revealed that Tslc1 null mice showed increases in the expression levels of genes involved in apoptosis, adhesion, and the cytoskeleton. Taken together, these data show that Tslc1 is essential for normal spermatogenesis in mice.

* Corresponding author. Mailing address: Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, United Kingdom, Phone: 44-1223-834-244. Fax: 44-1223-494-714. E-mail: abradley{at}sanger.ac.uk.

{dagger} Supplemental material for this article may be found at http://mcb.asm.org/.

Molecular and Cellular Biology, May 2006, p. 3595-3609, Vol. 26, No. 9
0270-7306/06/$08.00+0     doi:10.1128/MCB.26.9.3595-3609.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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