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Molecular and Cellular Biology, August 2005, p. 6346-6354, Vol. 25, No. 15
0270-7306/05/$08.00+0     doi:10.1128/MCB.25.15.6346-6354.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Mice Lacking the UBC4-testis Gene Have a Delay in Postnatal Testis Development but Normal Spermatogenesis and Fertility

Nathalie Bedard,¹ Pascal Hingamp,¹ Zhiyu Pang,¹ Andrew Karaplis,² Carlos Morales,³ Jacquetta Trasler,⁴ Dan Cyr,⁵ Claude Gagnon,⁶ and Simon S. Wing^1*

Polypeptide Laboratory, Department of Medicine, McGill University, Montreal, Quebec, Canada,¹ Lady Davis Institute for Medical Research, Sir Mortimer B. Davis Jewish General Hospital, Department of Medicine, McGill University, Montreal, Quebec, Canada,² Department of Anatomy and Cell Biology, McGill University, Montreal, Quebec, Canada,³ Departments of Pediatrics, Pharmacology, and Human Genetics, McGill University, Montreal, Quebec, Canada,⁴ Laboratoire de Toxicologie, Institut National de la Recherche en Santé, Pointe Claire, Quebec, Canada,⁵ Urology Research Laboratories, Department of Urology, Royal Victoria Hospital, McGill University, Montreal, Quebec, Canada⁶

Received 15 February 2006/ Returned for modification 7 April 2005/ Accepted 4 May 2005

Activation of ubiquitination occurs during spermatogenesis and is dependent on the induction of isoforms of the UBC4 family of ubiquitin-conjugating enzymes. The UBC4-testis isoform is testis specific, is induced in round spermatids, and demonstrates biochemical functions distinct from a ubiquitously expressed isoform UBC4-1. To explore further the function of UBC4-testis, mice bearing inactivation of this gene were produced. Homozygous (–/–) mice showed normal body growth and fertility. Although testis weight and morphology were normal in testes from adult mice, examination of young mice during the first wave of spermatogenesis revealed that testes were 10% smaller in weight at 40 and 45 days of age but had become normal at 65 days of age. Overall protein content, levels of ubiquitinated proteins, and ubiquitin-conjugating activity did not differ between wild-type and homozygous (–/–) mice. Spermatid number, as well as the motility of spermatozoa isolated from the epididymis, was also normal in homozygous (–/–) mice. To determine whether the germ cells lacking UBC4-testis might be more sensitive to stress, testes from wild-type and knockout mice were exposed to heat stress by implantation in the abdominal cavity. Testes from both strains of mice showed similar rates of degeneration in response to heat. The lack of an obvious phenotype did not appear to be due to induction of other UBC4 isoforms, as shown by two-dimensional gel immunoblotting. Our data indicate that UBC4-testis plays a role in early maturation of the testis and suggest that the many UBC4 isoforms have mixed redundant and specific functions.

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* Corresponding author. Mailing address: Polypeptide Laboratory, Department of Medicine, McGill University, Strathcona Anatomy and Dentistry Bldg., Rm. W315, 3640 University, Montreal, Quebec, Canada H3A 2B2. Phone: (514) 398-4101. Fax: (514) 398-3923. E-mail: simon.wing{at}mcgill.ca.

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Molecular and Cellular Biology, August 2005, p. 6346-6354, Vol. 25, No. 15
0022-538X/05/$08.00+0     doi:10.1128/MCB.25.15.6346-6354.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

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