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Published-Ahead-of-Print July 12, 2006, DOI:10.2164/jandrol.106.000398
Journal of Andrology, Vol. 27, No. 6, November/December 2006
Copyright © American Society of Andrology
DOI: 10.2164/jandrol.106.000398

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Tslc1 (Nectin-Like Molecule-2) Is Essential for Spermatozoa Motility and Male Fertility

EZEQUIEL I. SURACE*, AMY STRICKLAND{dagger}, REX A. HESS{ddagger}, DAVID H. GUTMANN* AND CATHY K. NAUGHTON{dagger}

From the * Department of Neurology and the {dagger} Department of Urologic Surgery, Washington University School of Medicine, St. Louis, Missouri; and the {ddagger} Department of Veterinary Biosciences, University of Illinois at Urbana-Champaign, Urbana, Illinois.

Correspondence to: Dr Cathy K. Naughton, Department of Surgery, Division of Urology, Washington University School of Medicine, 1040 North Mason Road, Suite 122, St. Louis, MO 63141 (e-mail: naughtonc{at}wustl.edu).


The nectin-like molecule-2 (TSLC1) is a cell-cell adhesion molecule expressed in testicular germ cells. To directly examine the role of Tslc1 in male fertility, we generated Tslc1+/– mice that have greater than 90% reduction in Tslc1 expression. Tslc1+/– males exhibited reduced fertility and rarely transmitted the Tslc1 mutant allele, whereas Tslc1+/– females were consistently able to transmit the mutant allele. Histologic and electron microscopic analyses of the testes in Tslc1+/– mice demonstrated disruption of the junctional scaffold between germ cells and Sertoli cells. Reduced Tslc1 expression had no effect on germ cell proliferation or apoptosis. While evidence of normal spermatozoal maturation was supported by Fluorescence Activated Cell Sorting (FACS) analysis, spermatozoa from Tslc1+/– mice demonstrated markedly reduced motility without compromised viability. Collectively, these results establish an essential role for Tslc1 in spermatozoal maturation and motility, distinct from other members of the nectin family.

     Key words: Spermatogenesis, spermiogenesis, testis, Syn-CAM1, IgSF4




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