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Molecular and Cellular Biology, April 2007, p. 2582-2589, Vol. 27, No. 7
0270-7306/07/$08.00+0     doi:10.1128/MCB.01722-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Abnormal Sperm in Mice Lacking the Taf7l Gene{triangledown} ,{dagger}

Yong Cheng,1 Mariano G. Buffone,2 Martin Kouadio,3 Mary Goodheart,4 David C. Page,4 George L. Gerton,2 Irwin Davidson,3 and Peijing Jeremy Wang1*

Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104,1 Center for Research on Reproduction and Women's Health, Department of Obstetrics and Gynecology, University of Pennsylvania Medical Center, Philadelphia, Pennsylvania 19104,2 Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/INSERM/ULP, 1 Rue Laurent Fries, 67404 Illkirch Cédex, France,3 Howard Hughes Medical Institute, Whitehead Institute, and Department of Biology, Massachusetts Institute of Technology, 9 Cambridge Center, Cambridge, Massachusetts 021424

Received 12 September 2006/ Returned for modification 30 October 2006/ Accepted 8 January 2007

TFIID is a general transcription factor required for transcription of most protein-coding genes by RNA polymerase II. TAF7L is an X-linked germ cell-specific paralogue of TAF7, which is a generally expressed component of TFIID. Here, we report the generation of Taf7l mutant mice by homologous recombination in embryonic stem cells by using the Cre-loxP strategy. While spermatogenesis was completed in Taf7l–/Y mice, the weight of Taf7l–/Y testis decreased and the amount of sperm in the epididymides was sharply reduced. Mutant epididymal sperm exhibited abnormal morphology, including folded tails. Sperm motility was significantly reduced, and Taf7l–/Y males were fertile with reduced litter size. Microarray profiling revealed that the abundance of six gene transcripts (including Fscn1) in Taf7l–/Y testes decreased more than twofold. In particular, FSCN1 is an F-action-bundling protein and thus may be critical for normal sperm morphology and sperm motility. Although deficiency of Taf7l may be compensated in part by Taf7, Taf7l has apparently evolved new specialized functions in the gene-selective transcription in male germ cell differentiation. Our mouse studies suggest that mutations in the human TAF7L gene might be implicated in X-linked oligozoospermia in men.


* Corresponding author. Mailing address: Dept. of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, 3800 Spruce Street, Philadelphia, PA 19104. Phone: (215) 746-0160. Fax: (215) 573-5188. E-mail: pwang{at}vet.upenn.edu.

{triangledown} Published ahead of print on 22 January 2007.

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


Molecular and Cellular Biology, April 2007, p. 2582-2589, Vol. 27, No. 7
0270-7306/07/$08.00+0     doi:10.1128/MCB.01722-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.




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