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Journal of Molecular Endocrinology (2005) 34 645-654    DOI: 10.1677/jme.1.01666
© 2005 Society for Endocrinology

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Disruption of the murine PIASx gene results in reduced testis weight

H Santti1, L Mikkonen1, A Anand1, S Hirvonen-Santti1, J Toppari3, M Panhuysen5, F Vauti5, M Perera6, G Corte5, W Wurst5, O A Jänne1,2 and J J Palvimo1,4

1 Biomedicum Helsinki, Institute of Biomedicine, University of Helsinki, FI-00014 Helsinki, Finland
2 Department of Clinical Chemistry, University of Helsinki, FI-00014 Helsinki, Finland
3 Departments of Physiology and Pediatrics, University of Turku, FI-20520 Turku, Finland
4 Department of Medical Biochemistry, University of Kuopio, FI-70211 Kuopio, Finland
5 Institute of Developmental Genetics, GSF-National Research Center for Environment and Health, Neuherberg, Germany
6 Laboratory of Gene Transfer, National Institute for Cancer Research and DOBIG, University of Genova, Genova, Italy

(Requests for offprints should be addressed to J J Palvimo; Email: jorma.palvimo{at}helsinki.fi)

PIASx belongs to the PIAS protein family, the members of which modulate activities of several transcription factors and act as E3 ligases in the sumoylation pathway. The PIASx gene is highly expressed in testis, suggesting a role in spermatogenesis. To investigate the function of PIASx in vivo, we have disrupted the PIASx gene in mice. Interestingly, the knockout mice were viable and fertile. Despite the normal fertility, the testis weight of the mutant animals was reduced and their number of apoptotic testicular cells was increased. Also, the sperm count of mutant mice tended to be reduced, but the quality of their sperm cells was normal. No significant changes were observed in the serum levels of LH and FSH or in the intratesticular testosterone concentration between the knockout animals and their wild-type littermates. Compensatory increases in other PIAS protein mRNAs were not observed in the knockout mice. These results imply that PIASx is required quantitatively rather than qualitatively for normal spermatogenesis.




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